Journal articles on the topic 'Corneal endothelium'

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1

Chirila, Traian V., Peter W. Madden, and Lawrie W. Hirst. "Replacement of the Corneal Endothelium and the Conceptual Framework for an Artificial Substitute." Journal of Biomimetics, Biomaterials and Tissue Engineering 5 (February 2010): 13–29. http://dx.doi.org/10.4028/www.scientific.net/jbbte.5.13.

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Dysfunction of the corneal endothelium due to cell loss caused by aging, disease or trauma can lead to severe visual impairment and blindness. Traditionally, dysfunctional endothelia are managed surgically, by removing the entire central cornea and transplanting either donor corneal tissue (penetrating keratoplasty), or just endothelia isolated from donor corneas. As in many cases it is only the corneal endothelium requiring replacement, many attempts were made over the last decades to develop an endothelial substitute, thereby precluding the need for the use of full donor corneas. This article reviews these attempts, which include artificial membranes, cell-coated corneal transplants, and cell-coated membranes. The presumption of an artificial corneal endothelium capable of duplicating the transendothelial ion-and-fluid transport function is examined in light of the latest hypotheses regarding the mechanism of this function.
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2

Ong, Keith. "SLT may compromise the corneal endothelium." Asian Journal of Ophthalmology 13, no. 3 (April 1, 2014): 80–85. http://dx.doi.org/10.35119/asjoo.v13i3.129.

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Purpose: Whitish spots are sometimes noted in the corneal endothelium after Selective Laser Trabeculoplasty (SLT). One wonders whether this could be laser burns to the corneal endothelium. To evaluate the corneal endothelium after SLT, corneal specular microscopy was performed before and after SLT.Method: 20 patients with open angle glaucoma, who had SLT in February-March 2012, had their corneal endothelium examined with specular microscopy before and after SLT.Results: 4 of the 20 patients showed numerous dark patches/spots on specular microscopy photographs of corneal endothelium after SLT. These dark patches/spots were found to have resolved by one month. 6 of the 20 patients showed few dark patches/spots after SLT. 10 patients had no significant dark patches/spots after SLT.Conclusion: The effect of SLT on the corneal endothelium is probably transient, and longterm effects probably negligible in normal corneas. However, in compromised corneas and corneas with pigment deposits on endothelium or reduced corneal endothelial transparency, there may be a risk of corneal endothelial compromise especially following repeated SLT. The results of this study highlight caution when deciding to do repeat SLT.
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3

Guimarães, Celeste B., Luciane Albuquerque, Marcela Torikachvili, Eduarda V. Vargas, Cecilia C. Dall’Agnol, Tanise C. Silva, and João A. T. Pigatto. "Effects of atracurium besylate on corneal endothelium of chickens: in vitro study." Pesquisa Veterinária Brasileira 39, no. 1 (January 2019): 70–74. http://dx.doi.org/10.1590/1678-5150-pvb-5595.

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ABSTRACT: The aim of this study was to investigate the acute effects of atracurium besylate on cellular damage in corneal endothelium of chickens. Twenty healthy chicken eyes were assigned to the following groups: Group 1 (G1), experimental group (n=10); and Group 2 (G2), control (n=10). Excised corneoscleral buttons were immediately placed on glass microscopy slides with endothelial region faced up. Corneal endothelium of eyes in G1 were covered with AB (0.2mL, 10mg/mL) for 3 min and then rinsed with balanced salt solution (BSS), while the corneal endothelium of eyes in G2 were covered with BBS for 3 min. Corneas from both groups were stained with alizarin red/trypan blue and visualized by light microscopy. Ten random photographs were taken from each cornea. The area of cellular damage was measured by software in all samples and cell loss of each group was averaged and compared. Endothelial area of denudation and Descemet’s membrane exposure were higher in G1 than G2. In conclusion, atracurium besylate induced an acute damage on corneal endothelium of chickens.
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4

Hussain, Noor Ahmed, Francisco C. Figueiredo, and Che J. Connon. "Use of biomaterials in corneal endothelial repair." Therapeutic Advances in Ophthalmology 13 (January 2021): 251584142110582. http://dx.doi.org/10.1177/25158414211058249.

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Human corneal endothelium (HCE) is a single layer of hexagonal cells that lines the posterior surface of the cornea. It forms the barrier that separates the aqueous humor from the rest of the corneal layers (stroma and epithelium layer). This layer plays a fundamental role in maintaining the hydration and transparency of the cornea, which in turn ensures a clear vision. In vivo, human corneal endothelial cells (HCECs) are generally believed to be nonproliferating. In many cases, due to their nonproliferative nature, any damage to these cells can lead to further issues with Descemet’s membrane (DM), stroma and epithelium which may ultimately lead to hazy vision and blindness. Endothelial keratoplasties such as Descemet’s stripping automated endothelial keratoplasty (DSAEK) and Descemet’s membrane endothelial keratoplasty (DEK) are the standard surgeries routinely used to restore vision following endothelial failure. Basically, these two similar surgical techniques involve the replacement of the diseased endothelial layer in the center of the cornea by a healthy layer taken from a donor cornea. Globally, eye banks are facing an increased demand to provide corneas that have suitable features for transplantation. Consequently, it can be stated that there is a significant shortage of corneal grafting tissue; for every 70 corneas required, only 1 is available. Nowadays, eye banks face long waiting lists due to shortage of donors, seriously aggravated when compared with previous years, due to the global COVID-19 pandemic. Thus, there is an urgent need to find alternative and more sustainable sources for treating endothelial diseases, such as utilizing bioengineering to use of biomaterials as a remedy. The current review focuses on the use of biomaterials to repair the corneal endothelium. A range of biomaterials have been considered based on their promising results and outstanding features, including previous studies and their key findings in the context of each biomaterial.
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5

Andrade, M. C. C., T. M. Moreno, M. S. Muccillo, J. A. T. Pigatto, and E. V. Camilo. "Evaluation of equine corneal endothelium after exposure to 0.05% brilliant blue - an in vitro study." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 71, no. 4 (August 2019): 1158–64. http://dx.doi.org/10.1590/1678-4162-9969.

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ABSTRACT The aim of this study was to evaluate the immediate effects of 0.05% brilliant blue on corneal endothelium of horses. Thirty-eight corneas of 19 horses, male or female, of different ages were studied. Corneas were randomly divided into two groups. Group 1: Corneal endothelium was covered with 0.3mL of brilliant blue 0.05% for 60 seconds followed by rinsing with a balanced salt solution. Group 2: Corneal endothelium was covered with BSS for 60 seconds. The corneas were excised with an 8mm trephine and prepared to analyze posterior endothelial surface using a light microscope (24 corneas) and a scanning electron microscope (14 corneas). The equine posterior corneal endothelium surface observed by optical microscopy and scanning electron microscopy revealed a continuous layer of polygonal cells of uniform size and shape in both the control and treatment groups. Due to non-normal residuals at ANOVA mean comparison, a generalized linear model was utilized at 5% level of significance. The chi-square test stated that treatment and control group were not different statistically. The 0.05% brilliant blue did not cause damage to equine corneal endothelium.
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6

Wang, Xuemei, Yanlin Zhong, Minghui Liang, Zhirong Lin, Huping Wu, and Cheng Li. "Crosslinking-Induced Corneal Endothelium Dysfunction and Its Protection by Topical Ripasudil Treatment." Disease Markers 2022 (January 13, 2022): 1–12. http://dx.doi.org/10.1155/2022/5179247.

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Purpose. To investigate the changes of corneal endothelium under different crosslinking conditions and the protective effect of ripasudil. Methods. Corneal crosslinking groups were infiltrated with riboflavin and subsequently irradiated with 0.54 J/cm2 or 1.08 J/cm2 UVA, while noncrosslinking groups included neither UVA nor riboflavin treatment, only 1.08 J/cm2 UVA and only riboflavin treatment. Corneal opacity, variations in corneal endothelial cells, and corneal thickness of all groups were observed by slit lamp, in vivo confocal microscopy, and optical coherence tomography. Immunofluorescence staining and scanning electron microscopy were performed to evaluate changes in the structure and function of the corneal endothelium. The mice that received a corneal crosslinking dose of 1.08 J/cm2 were instilled with ripasudil to explore its protective effect on the corneal endothelium. Results. Treatment with UVA and riboflavin caused an increase in corneal opacity and corneal thickness and decreased endothelial cell density. Furthermore, treatment with UVA and riboflavin caused endothelial cell DNA damage and destroyed the tight junction and pump function of the endothelium, while riboflavin or the same dose of UVA alone did not affect the endothelium. Ripasudil reduced DNA damage in endothelial cells, increased the density of cells, and protected the endothelium’s integrity and function. Conclusion. Riboflavin combined with UVA can damage the corneal endothelium’s normal functioning. The corneal endothelium’s wound healing is dose-dependent, and the ROCK inhibitor ripasudil maintains the endothelium’s pump and barrier functions.
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7

Terzariol, Mariana, Paula S. Hünning, Gustavo Brambatti, Luciane de Albuquerque, Carolina Neumann, and João A. T. Pigatto. "Effects of intracameral brilliant blue on the corneal endothelium of swine: in vitro study." Pesquisa Veterinária Brasileira 36, no. 8 (August 2016): 775–80. http://dx.doi.org/10.1590/s0100-736x2016000800016.

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Abstract: The aim was to investigate the ultrastructural changes in the corneal endothelium of pigs induced by intracameral 0.05% brilliant blue. Twenty swine corneas were separated into two groups, the right eye bulbs (control group) and the left eye bulbs (experimental group) of the same animal. All the eye bulbs were evaluated with specular microscopy. The cornea of the right eye bulbs was excised and in the left eye bulbs 0.2ml of 0.05% brilliant blue vital dye (OPTH-blue±) was injected into the anterior chamber, where it remained for one minute. Then the anterior chamber was cleaned with a balanced salt solution injection and the cornea was excised too. All the corneas were evaluated by scanning electron microscopy to evaluate the changes on the endothelium caused by the brilliant blue dye. There were no significant differences between the right corneal endothelium cells and the left corneal endothelium cells with scanning electron microscopy after intracameral use of 0.05% brilliant blue dye. The 0.05% brilliant blue dye concentration did not cause deleterious effects for the swine corneal endothelium after intracameral use and can be a choice for safe staining of the anterior capsule of the lens in cataract surgery.
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8

Feizi, Sepehr. "Corneal endothelial cell dysfunction: etiologies and management." Therapeutic Advances in Ophthalmology 10 (January 2018): 251584141881580. http://dx.doi.org/10.1177/2515841418815802.

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A transparent cornea is essential for the formation of a clear image on the retina. The human cornea is arranged into well-organized layers, and each layer plays a significant role in maintaining the transparency and viability of the tissue. The endothelium has both barrier and pump functions, which are important for the maintenance of corneal clarity. Many etiologies, including Fuchs’ endothelial corneal dystrophy, surgical trauma, and congenital hereditary endothelial dystrophy, lead to endothelial cell dysfunction. The main treatment for corneal decompensation is replacement of the abnormal corneal layers with normal donor tissue. Nowadays, the trend is to perform selective endothelial keratoplasty, including Descemet stripping automated endothelial keratoplasty and Descemet’s membrane endothelial keratoplasty, to manage corneal endothelial dysfunction. This selective approach has several advantages over penetrating keratoplasty, including rapid recovery of visual acuity, less likelihood of graft rejection, and better patient satisfaction. However, the global limitation in the supply of donor corneas is becoming an increasing challenge, necessitating alternatives to reduce this demand. Consequently, in vitro expansion of human corneal endothelial cells is evolving as a sustainable choice. This method is intended to prepare corneal endothelial cells in vitro that can be transferred to the eye. Herein, we describe the etiologies and manifestations of human corneal endothelial cell dysfunction. We also summarize the available options for as well as recent developments in the management of corneal endothelial dysfunction.
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9

Baturina, G. S., I. G. Palchikova, A. A. Konev, E. S. Smirnov, L. E. Katkova, E. I. Solenov, and I. А. Iskakov. "STUDY OF THE EFFECT OF HYPOTHERMIC CONSERVATION ON THE INTRACELLULAR SODIUM CONCENTRATION IN THE ENDOTHELIUM OF CORNEAL TRANSPLANTS." Vavilov Journal of Genetics and Breeding 22, no. 4 (July 3, 2018): 433–37. http://dx.doi.org/10.18699/vj18.379.

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Endothelial keratoplasty has become the treatment of choice for corneal endothelial dysfunction. Advancements in the surgical treatment of corneal endothelial diseases depend on progress in graft conservation and its related advantages in assessing the suitability of grafts for transplantation. Transport of water and ions by cornea endothelium is important for the optic properties of cornea. In this work, we study the intracellular sodium concentration in cornea endothelial cells in samples of pig cornea that underwent hypothermic conservation for 1 and 10 days and endothelial cells of human cornea grafts after 10-day conservation. The concentration of intracellular sodium in preparations of endothelial cells was assayed using fluorescent dye SodiumGreen. The fluorescent images were analyzed with the custom-made computer program CytoDynamics. An increased level of intracellular sodium was shown in the endothelium after 10-day conservation in comparison with one-day conservation (pig samples). Sodium permeability of pig endothelial cell plasma membranes significantly decreased in these samples. Assessment of intracellular sodium in human cornea endothelium showed a higher level – as was in analogues pig samples of the corneal endothelium. The assay of the intracellular sodium balance concentration established in endothelial cells after hypothermic conservation in mediums L-15 and Optisol-GS showed a significant advantage of specialized me dium Optisol-GS. The balanced intracellular concentration after 10 days of hypothermic conservation was significantly lower in cells incubated at 4 °C in Optisol-GS (L-15, 128 ± 14, n = 15; Optisol-GS, 108 ± 14, n = 11; mM, p < 0.001). Intracellular sodium concentration could be a useful parameter for assessing cornea endothelium cell viability.
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10

Bryant, M. R., and P. J. McDonnell. "A Triphasic Analysis of Corneal Swelling and Hydration Control." Journal of Biomechanical Engineering 120, no. 3 (June 1, 1998): 370–81. http://dx.doi.org/10.1115/1.2798004.

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Physiological studies strongly support the view that hydration control in the cornea is dependent on active ion transport at the corneal endothelium. However, the mechanism by which endothelial ion transport regulates corneal thickness has not been elaborated in detail. In this study, the corneal stroma is modeled as a triphasic material under steady-state conditions. An ion flux boundary condition is developed to represent active transport at the endothelium. The equations are solved in cylindrical coordinates for confined compression and in spherical coordinates to represent an intact cornea. The model provides a mechanism by which active ion transport at the endothelium regulates corneal hydration and provides a basis for explaining the origin of the “imbibition pressure” and stromal “swelling pressure.” The model encapsulates the Donnan view of corneal swelling as well as the “pump-leak hypothesis.”
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11

Zhao, Can, Wenjing Li, Haoyun Duan, Zongyi Li, Yanni Jia, Songmei Zhang, Xin Wang, Qingjun Zhou, and Weiyun Shi. "NAD+ precursors protect corneal endothelial cells from UVB-induced apoptosis." American Journal of Physiology-Cell Physiology 318, no. 4 (April 1, 2020): C796—C805. http://dx.doi.org/10.1152/ajpcell.00445.2019.

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Excessive exposure of the eye to ultraviolet B light (UVB) leads to corneal edema and opacification because of the apoptosis of the corneal endothelium. Our previous study found that nicotinamide (NIC), the precursor of nicotinamide adenine dinucleotide (NAD), could inhibit the endothelial-mesenchymal transition and accelerate healing the wound to the corneal endothelium in the rabbit. Here we hypothesize that NIC may possess the capacity to protect the cornea from UVB-induced endothelial apoptosis. Therefore, a mouse model and a cultured cell model were used to examine the effect of NAD+ precursors, including NIC, nicotinamide mononucleotide (NMN), and NAD, on the UVB-induced apoptosis of corneal endothelial cells (CECs). The results showed that UVB irradiation caused apparent corneal edema and cell apoptosis in mice, accompanied by reduced levels of NAD+ and its key biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT), in the corneal endothelium. However, the subconjunctival injection of NIC, NMN, or NAD+ effectively prevented UVB-induced tissue damage and endothelial cell apoptosis in the mouse cornea. Moreover, pretreatment using NIC, NMN, and NAD+ increased the survival rate and inhibited the apoptosis of cultured human CECs irradiated by UVB. Mechanistically, pretreatment using nicotinamide (NIC) recovered the AKT activation level and decreased the BAX/BCL-2 ratio. In addition, the capacity of NIC to protect CECs was fully reversed in the presence of the AKT inhibitor LY294002. Therefore, we conclude that NAD+ precursors can effectively prevent the apoptosis of the corneal endothelium through reactivating AKT signaling; this represents a potential therapeutic approach for preventing UVB-induced corneal damage.
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12

Рыков, С. А., М. Г. Лысенко, И. В. Шаргородская, Н. С. Лаврик, И. А. Макаренко, Л. П. Новак, and С. В. Выдыборец. "Endothelial Cells Survival in Human Corneal Grafts When Using the Modified Method Treatment of Keratoconus." Офтальмология. Восточная Европа, no. 3 (November 27, 2020): 311–27. http://dx.doi.org/10.34883/pi.2020.10.3.019.

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Проведена лазерная сканирующая конфокальная микроскопия донорских трупных роговиц, предназначенных для кератопластики. С помощью программного обеспечения ImageJ проанализирована рефлективность эндотелия и введено понятие коэффициента рефлективности эндотелиальных клеток роговицы (КРЭКР). В ходе статистической обработки определены морфометрические свойства эндотелиоцитов при конфокальной микроскопии, которые существенно влияют на потерю эндотелиальных клеток на трансплантате и, возможно, являются признаками апоптоза эндотелиоцитов. Разработана методика вископротекции эндотелия кадаверной роговицы на этапе формирования трансплантата. Отмечено, что сочетание качественной отбраковки донорского роговичного материала по разработанным критериям с проведением интраоперационной вископротекции эндотелия сокращает процент потери эндотелиальных клеток на роговичном трансплантате почти в 4 раза в течение первого года после трансплантации, что является профилактикой развития позднего эндотелиального отторжения роговичного трансплантата. Установлено, что общий (абсолютный и относительный) брак донорских роговиц для проведения сквозной аллокератопластики при кератоконусе составляет приблизительно 60%. Keratoconus is a disorder of the eye characterized by thinning and protrusion of the cornea, resulting in an irregular, conical shape and is the cause of persistent decline in vision and disability of young able-bodied people. Despite development of lamellar techniques of corneal surgery, penetrating keratoplasty remains the "gold standard" in the keratoconus treatment. The rapid loss of endothelial cells on the corneal graft at 6 months after keratoplasty is an important early symptom of late graft rejection (Lass J.H. et all, 2010). The aim of this study is to improve the quality of preservation ofendothelial cells on the native corneal grafts. This task can be solved by qualitative preliminary selection of donor tissue and reduction of intraoperative traumatization of endothelium on corneal graft.Methods. In Kyiv ophthalmic city hospital "Eye microsurgery center" (Kyiv, Ukraine) determined preoperative endothelium cells density by Heidelberg Retina Tomograph HRT II Rostock Cornea Module and were archived available endothelium cells images (590 human cadaveric corneas). Endothelial cells reflectivity analyses performed by ImageJ free software. Proposed to introduce the concept of the coefficient of reflectivity of corneal endothelial cells. Also noted the presence of organelles and "swelling" endothelial cells.In 1st clinic group (n=57) all the patients got standard penetrating keratoplasty procedure with standardly graft exams. Investigated the dependence of rapid endothelial cells loss with endothelial morphometric properties. In 2nd clinic group (n=29) all the patients got standard penetrating keratoplasty procedure with qualitative screening of corneas with new morphometric criteria (coefficient of corneal endothelial reflectivity more, than 50; without "swelling" endothelial cells and without organelles in the endothelial cells). In 3rd clinic group (n=43) patients got qualitative screening of corneas (like 2nd group), but viscoprotection during "back table" procedure has been developed.Results. As a result, combination of qualitative rejection of cadaveric corneas with morphometric endothelial factors reduces the percentage of cell loss four times. Tree morphometric factors in any combination were related with rapid loss of endothelial cells in graft: coefficient of corneal endothelial reflectivity lower, than 50; "swelling" endothelial cells and organelles in the endothelial cells. Determined that total (absolute and relative) qualitative rejection make unsuitable for penetrating keratoplasty for keratoconus approximately 60% of cadaveric corneas.Discussion. This study may help to reduce endothelial cells loss and frequency of late endothelial rejection of corneal grafts. Tree morphometric factors in any combination were related with rapid loss of endothelial cells in graft: coefficient of corneal endothelial reflectivity lower, than 50; "swelling" endothelial cells and organelles in the endothelial cells. Perhaps, these factors are markers of endothelial cells apoptosis.Conclusion. Investigated the dependence of rapid endothelial cells loss with endothelial morphometric properties. Proposed to introduce the concept of the coefficient of reflectivity of corneal endothelial cells. Proposed the methodology of endothelial viscoprotection during "back table" procedure before penetrating keratoplasty.
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13

Lovatt, Matthew, Khadijah Adnan, Gary Peh, and Jodhbir Mehta. "Regulation of Oxidative Stress in Corneal Endothelial Cells by Prdx6." Antioxidants 7, no. 12 (December 4, 2018): 180. http://dx.doi.org/10.3390/antiox7120180.

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The inner layer of the cornea, the corneal endothelium, is post-mitotic and unable to regenerate if damaged. The corneal endothelium is one of the most transplanted tissues in the body. Fuchs’ endothelial corneal dystrophy (FECD) is the leading indication for corneal endothelial transplantation. FECD is thought to be an age-dependent disorder, with a major component related to oxidative stress. Prdx6 is an antioxidant with particular affinity for repairing peroxidised cell membranes. To address the role of Prdx6 in corneal endothelial cells, we used a combination of biochemical and functional studies. Our data reveal that Prdx6 is expressed at unusually high levels at the plasma membrane of corneal endothelial cells. RNAi-mediated knockdown of Prdx6 revealed a role for Prdx6 in lipid peroxidation. Furthermore, following induction of oxidative stress with menadione, Prdx6-deficient cells had defective mitochondrial membrane potential and were more sensitive to cell death. These data reveal that Prdx6 is compartmentalised in corneal endothelial cells and has multiple functions to preserve cellular integrity.
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Sun, Xing Cai, Joseph A. Bonanno, Sergey Jelamskii, and Qiang Xie. "Expression and localization of Na+-HCO3 − cotransporter in bovine corneal endothelium." American Journal of Physiology-Cell Physiology 279, no. 5 (November 1, 2000): C1648—C1655. http://dx.doi.org/10.1152/ajpcell.2000.279.5.c1648.

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Functional studies support the presence of the Na+-HCO3 −cotransporter (NBC) in corneal endothelium and possibly corneal epithelium; however, molecular identification and membrane localization have not been reported. To test whether NBC is expressed in bovine cornea, Western blotting was performed, which showed a single band at ∼130 kDa for freshly isolated and cultured endothelial cells, but no band for epithelium. Two isoforms of NBC have recently been cloned in kidney (kNBC) and pancreas (pNBC). RT-PCR was run using cultured and fresh bovine corneal endothelial and fresh corneal epithelial total RNA and specific primers for kNBC and pNBC. RT-PCR analysis for pNBC was positive in endothelium and weak in epithelium. The RT-PCR product was subcloned and confirmed as pNBC by sequencing. No specific bands for kNBC were obtained from corneal cells. Indirect immunofluorescence and confocal microscopy indicated that NBC locates predominantly to the basolateral membrane in corneal endothelial cells. Furthermore, Na+-dependent HCO3 − fluxes and HCO3 −-dependent cotransport with Na+ were elicited only from the basolateral side of corneal endothelial cells. Therefore, we conclude that pNBC is present in the basolateral membrane of both fresh and cultured bovine corneal endothelium and weakly expressed in the corneal epithelium.
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Vallabh, Neeru A., Stephnie Kennedy, Riccardo Vinciguerra, Keri McLean, Hannah Levis, Davide Borroni, Vito Romano, and Colin E. Willoughby. "Corneal Endothelial Cell Loss in Glaucoma and Glaucoma Surgery and the Utility of Management with Descemet Membrane Endothelial Keratoplasty (DMEK)." Journal of Ophthalmology 2022 (January 30, 2022): 1–17. http://dx.doi.org/10.1155/2022/1315299.

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The corneal endothelium has a crucial role in maintaining a clear and healthy cornea. Corneal endothelial cell loss occurs naturally with age; however, a diagnosis of glaucoma and surgical intervention for glaucoma can exacerbate a decline in cell number and impairment in morphology. In glaucoma, the mechanisms for this are not well understood, and this accelerated cell loss can result in corneal decompensation. Given the high prevalence of glaucoma worldwide, this review aims to explore the abnormalities observed in the corneal endothelium in differing glaucoma phenotypes and glaucoma therapies (medical or surgical, including with new generation microinvasive glaucoma surgeries). Descemet membrane endothelial keratoplasty (DMEK) is increasingly being used to manage corneal endothelial failure for glaucoma patients, and we aim to review the recent literature evaluating the use of this technique in this clinical scenario.
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Wang, De-An, Haiming Du, Jonathan H. Jaggar, David N. Brindley, Gabor J. Tigyi, and Mitchell A. Watsky. "Injury-elicited differential transcriptional regulation of phospholipid growth factor receptors in the cornea." American Journal of Physiology-Cell Physiology 283, no. 6 (December 1, 2002): C1646—C1654. http://dx.doi.org/10.1152/ajpcell.00323.2002.

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The phospholipid growth factors (PLGFs), including lysophosphatidic acid (LPA), have been implicated in corneal wound healing. PLGF concentrations and activities are elevated after corneal injury. Using real-time PCR, we quantified receptor mRNA levels in the healing rabbit cornea. In intact corneas, transcripts for S1P1, LPA1, and LPA3 receptor subtypes were detected, as was lipid phosphate phosphatase 1 (LPP1). After wounding, the trend for endothelium and keratocytes was for significant decreases in transcript numbers for the three receptor subtypes, whereas epithelial cells showed increased transcript numbers, except for an S1P1 decrease in healing cells. LPP1 transcript numbers were decreased in keratocytes and endothelium, although LPP-specific activity was unchanged. LPA-elicited Ca2+ transients were significantly reduced in the healing endothelium. Consistent with reduced LPA3 receptor numbers, dioctylglycerol pyrophosphate, a selective antagonist, reduced LPA-induced Ca2+ transients 2.7-fold in nonwounded epithelium but only 1.5-fold in wound-healing endothelium. These data for the first time establish physiologically relevant differential changes in the expression of PLGF receptor subtypes and provide evidence for the changing role of LPA3 receptors in endothelial cells.
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Tang, Q., and R. L. Hendricks. "Interferon gamma regulates platelet endothelial cell adhesion molecule 1 expression and neutrophil infiltration into herpes simplex virus-infected mouse corneas." Journal of Experimental Medicine 184, no. 4 (October 1, 1996): 1435–47. http://dx.doi.org/10.1084/jem.184.4.1435.

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In a mouse model of herpes simplex virus (HSV) 1 corneal infection, tissue destruction results from a CD4+ T cell-mediated chronic inflammation, in which interleukin 2 and interferon (IFN) gamma are requisite inflammatory mediators and polymorphonuclear leukocytes (PMN) are the predominant infiltrating cells. In vivo neutralization of IFN-gamma relieved inflammation at least in part through a specific block of PMN extravasation into HSV-1-infected corneas. Intercellular adhesion molecule (ICAM) 1 and platelet endothelial cell adhesion molecule (PECAM) 1 were upregulated on the vascular endothelium of inflamed corneas. Reduced PMN extravasation in anti-IFN-gamma-treated mice was associated with a dramatic reduction of PECAM-1 but not ICAM-1 expression on vascular endothelium. PMN accumulated in the lumen of corneal vessels after in vivo IFN-gamma neutralization. PECAM-1 was readily detectable on PMN inside the vessels but was not detectable on PMN that extravasated into the infected cornea. Moreover, flow cytometric analysis revealed reduced PECAM-1 expression but elevated major histocompatibility complex class I expression on PMN that recently extravasated into the peritoneal cavity when compared with PMN in the peripheral blood. We conclude that IFN-gamma contributes to HSV-1-induced corneal inflammation by facilitating PMN infiltration; this appears to be accomplished through upregulation of PECAM-1 expression on the vascular endothelium; and PMN downregulate PECAM-1 expression during the process of extravasation.
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18

Yam, Seah, Yusoff, Setiawan, Wahlig, Htoon, Peh, Kocaba, and Mehta. "Characterization of Human Transition Zone Reveals a Putative Progenitor-Enriched Niche of Corneal Endothelium." Cells 8, no. 10 (October 12, 2019): 1244. http://dx.doi.org/10.3390/cells8101244.

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: The corneal endothelium regulates corneal hydration to maintain the transparency of cornea. Lacking regenerative capacity, corneal endothelial cell loss due to aging and diseases can lead to corneal edema and vision loss. There is limited information on the existence of corneal endothelial progenitors. We conducted ultrastructural examinations and expression analyses on the human transition zone (TZ) at the posterior limbus of corneal periphery, to elucidate if the TZ harbored progenitor-like cells, and to reveal their niche characteristics. Within the narrow TZ (~190 μm width), the inner TZ—adjacent to the peripheral endothelium (PE)—contained cells expressing stem/progenitor markers (Sox2, Lgr5, CD34, Pitx2, telomerase). They were located on the inner TZ surface and in its underlying stroma. Lgr5 positive cells projected as multicellular clusters into the PE. Under transmission electron microscopy and serial block face-scanning electron microscopy and three-dimensional (3D) reconstruction, the terminal margin of Descemet’s membrane was inserted beneath the TZ surface, with the distance akin to the inner TZ breadth. Porcine TZ cells were isolated and proliferated into a confluent monolayer and differentiated to cells expressing corneal endothelial markers (ZO1, Na+K+ATPase) on cell surface. In conclusion, we have identified a novel inner TZ containing progenitor-like cells, which could serve the regenerative potential for corneal endothelium.
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Singasandra, Sanjana Marijogaiah, Radhika Srinivasagupta Mohan, Dakshayini Mallaiah, and Shwetha Bennavara Venkataswamy. "A comparative study of endothelial cell loss in small incision cataract surgery versus phacoemulsification cataract surgery by using specular microscope at tertiary care ophthalmic centre in Bengaluru, Karnataka." IP International Journal of Ocular Oncology and Oculoplasty 7, no. 4 (February 15, 2022): 399–405. http://dx.doi.org/10.18231/j.ijooo.2021.084.

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Most commonly performed surgical procedure in Ophthalmology is cataract extraction by MSICS and Phacoemulsification. It has always been associated with damage to endothelium of cornea, a layer which is vital for maintaining corneal transparency. The corneal endothelium regulates stromal hydration and maintains the transparency of the cornea by constantly removing the fluid out of the corneal stroma. The density of corneal endothelial cells and its integrity is an important determinant for corneal transparency. Post-operative corneal decompensation leading to reduced visual acuity can occur as a result of this surgical trauma. Hence it is necessary to determine the surgical technique safest to corneal endothelium. Specular microscopy helps to determine this corneal endothelial cell density. A hospital based longitudinal study was done from November 2017 to May 2019 in 124 patients at Minto Ophthalmic Hospital. 62 patients underwent MSICS and 62 phacoemulsification. After a written informed consent patients were evaluated with detailed history, slit lamp examination, direct and indirect ophthalmoscopy, biometry, lacrimal syringing, IOP measurement with tonometry and endothelial cell count was evaluated using non contact specular microscopy preoperatively and postoperative 1 week and 6 weeks. Statistical data analysed by unpaired – t test. The mean ECC (cells/mm) in MSICS and phacoemulsification group preoperatively was 2486.82 + 152.730 and 2433.71 + 192.692 respectively. The mean endothelial cell loss (cells/mm) was 314.61 + 64.428 and 324.31 + 30.67 at 1 week and 345.71 + 66.68 and 354.95 + 53.885 at 6 weeks postoperatively between the two groups. The endothelial cell loss was not statistically significant at 1 week (p -0.28) and 6 weeks (p-0.39) postoperatively between the two groups. There was no clinically or statistically significant difference in the endothelial cell loss between MSICS and Phacoemulsification. As MSICS is economical and less dependent on technology, it can be a safe option in developing world.
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Ganekal, Sunil, and Varun Ganekal. "Anterior capsule sparing parsplana lensectomy in cataract with severely compromised corneal endothelium." Indian Journal of Clinical and Experimental Ophthalmology 8, no. 2 (June 15, 2022): 224–27. http://dx.doi.org/10.18231/j.ijceo.2022.045.

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To evaluate the results of parsplana lensectomy in the management of cataract with severely compromised or abnormal corneal endothelium. Retrospective interventional case study comprised 22 patients (9 women, 13 men; 22 eyes) with severely abnormal corneal endothelium ut still had transparent cornea. Of which 14 had history of penetrating keratoplasty, 6 had history of trabeculectomy and 2 were diagnosed with Fuch’s endothelial dystrophy. Postoperative est corrected visual acuity (BCVA), mean density of corneal endothelial cell and other complications were analyzed. Mean follow-up period was 17.2 months (ranging from 6 to 31 months). Postoperative BCVA were found to be 6/60 or below in 2 patients, 6/60-6/18 in 7 patients and 6/18-6/12 in 7 patients and 6/12 or better in 6 patients. BCVA improved in all patients after surgery, except in one patient with Fuch’s endothelial dystrophy BCVA turned worse again about five months after surgery and eventually patient developed bullous keratopathy. The mean density of corneal endothelial cells was 1018± 84/ mm (range 844/ mm to 1176/ mm) before operation and 981±93/ mm (range 853 to 1211/ mm) after operation. No significant difference in the density of corneal endothelial cells was found among the patients before and after operation (P=0.43).Pars plana lensectomy is able to decrease surgically-induced corneal endothelial damage and is safe in the management of cataract with severely compromised corneal endothelium.
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Yildirim, Timur Mert, Gerd U. Auffarth, Hyeck-Soo Son, Ramin Khoramnia, Donald John Munro, and Patrick R. Merz. "Dispersive viscosurgical devices demonstrate greater efficacy in protecting corneal endothelium in vitro." BMJ Open Ophthalmology 4, no. 1 (February 2019): e000227. http://dx.doi.org/10.1136/bmjophth-2018-000227.

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ObjectiveDuring phacoemulsification, the corneal endothelium is protected by an ophthalmic viscosurgical device (OVD). In this in vitro study, we assessed six different OVDs for their effectiveness in protecting the corneal endothelium.Methods and analysisPhacoemulsification was performed in cadaver eyes of young pigs. Five syringe units of six different OVDs were tested (Healon EndoCoat, Viscoat, Methylvisc, Healon, Healon GV, ProVisc). After surgery, the area of endothelium coated with OVD was determined in relation to the total endothelial surface. Additionally, an endothelial cell count was obtained. As a control, an endothelial cell count was obtained from freshly trephined corneas. Statistical analysis was performed using the Mann-Whitney U test and the Spearman correlation.ResultsThe least postoperative endothelial coating and cell count were observed in the cohesive OVDs while the dispersive OVDs showed statistically significant higher values. Healon EndoCoat and Viscoat yielded a coating area of 86 (85–92)% and 85 (85-90)%, respectively. Endothelial cell count was highest in the two dispersive groups with 4065 (3928–4088) cells/mm2 (Methylvisc) and 4032 (4015–4115) cells/mm2 (Viscoat). Endothelial coating area and endothelial cell count correlated statistically significantly.ConclusionDispersive OVDs from this study showed greater adherence to the endothelial surface than the cohesive ones. Furthermore, postoperative endothelial cell counts of corneas treated with dispersive OVDs were higher than of corneas treated with cohesive OVDs. Our in vitro results suggest that dispersive OVDs protect the corneal endothelium better during phacoemulsification than cohesive OVDs.
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Reinstein Merjava, Stanislava, Jan Kossl, Ales Neuwirth, Pavlina Skalicka, Zuzana Hlinomazova, Vladimir Holan, and Katerina Jirsova. "Presence of Protease Inhibitor 9 and Granzyme B in Healthy and Pathological Human Corneas." Biology 11, no. 5 (May 23, 2022): 793. http://dx.doi.org/10.3390/biology11050793.

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The aim of this study was to find out whether protease inhibitor 9 (PI-9) and granzyme B (GrB) molecules that contribute to immune response and the immunological privilege of various tissues are expressed in healthy and pathological human corneas. Using cryosections, cell imprints of control corneoscleral discs, we showed that PI-9 was expressed particularly in the endothelium, the superficial and suprabasal epithelium of healthy corneas, limbus, and conjunctiva. GrB was localized in healthy corneal and conjunctival epithelium, while the endothelium showed weak immunostaining. The expression of PI-6 and GrB was confirmed by qRT-PCR. Increased expression levels of the PI-9 and GrB genes were determined when the corneas were cultured with proinflammatory cytokines. Fluorescent and enzymatic immunohistochemistry of pathological corneal explants (corneal melting and herpes virus keratitis) showed pronounced PI-9, GrB, human leucocyte antigen (HLA)-DR, and leukocyte-common antigen (CD45) signals localized in multicellular stromal infiltrates and inflammatory cells scattered in the corneal stroma. We conclude that increased expression of the PI-9 and GrB proteins under pathological conditions and their upregulation in an inflammatory environment indicate their participation in immune response of the cornea during the inflammatory process.
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Watsky, M. A. "Nonselective cation channel activation during wound healing in the corneal endothelium." American Journal of Physiology-Cell Physiology 268, no. 5 (May 1, 1995): C1179—C1185. http://dx.doi.org/10.1152/ajpcell.1995.268.5.c1179.

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Rabbit corneas were injured by mechanical or thermal trauma. At several time points after wounding, corneal endothelial cells were isolated and their ion channels examined using standard and amphotericin perforated-patch whole cell patch-clamp configurations. Within 15-24 h after mechanical or thermal trauma, a nonselective cation current was observed in 79% of the cells examined that was not present in unwounded or sham-wounded corneas. By 73 h postwounding, the current was present in only 10% of the cells examined. The wound healing-induced current is outwardly rectifying, activates at depolarized voltages, shows no sign of inactivation, and is inhibited by flufenamic acid, quinidine, and acetate. In addition to this new current, it was observed that endothelial cells from freeze-wounded corneas no longer expressed the transient K+ current seen in control, sham, and mechanically wounded corneas. Corneal endothelial superfusion experiments found no significant difference in swelling rates between control and flufenamic acid-superfused wounded corneas, indicating that the wound healing-induced channel is not involved in the stromal hydration maintenance function of the corneal endothelium.
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Fisenko, N. V. "Cornea: anatomical and functional features, new methods of in vivo diagnostics of abnormalities." Journal of Anatomy and Histopathology 11, no. 2 (June 30, 2022): 78–86. http://dx.doi.org/10.18499/2225-7357-2022-11-2-78-86.

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The cornea is a highly organized, transparent part of fibrous tunic of an eyeball. It acts as the primary infectious and structural barrier of the eye. The cornea is the major refractive element of an adult eye. It consists of epithelium, Bowman's membrane, stroma, Descemet's membrane and endothelium. Although the normal human cornea is avascular, it is supplied via perilimbal blood vessels, the aqueous humor (AqH) and tear film. Afferent innervation to the cornea is provided by long ciliary nerves, which form subepithelial and subbasal nerve plexus. Epithelium is a stratified, non-keratinizing squamous layer that consists of various cell types. Epithelial cells are connected to each other by zonula adherens, and to the basement membrane via hemidesmosomes. Bowman's membrane is composed of randomly-oriented type I and V collagen fibrils and anchoring type IV and VII collagen fibrils. The stroma consists of cells (principally keratocytes) and distinct lamella formed by collagen fibers, proteoglycans, elastin and glycoproteins. Descemet's membrane is a basal membrane, secreted by endothelial cells. It is a network organized by type VIII collagen molecules, which modulate the passage of growth factors, cytokines and nutrients from the AqH into the corneal stroma and backward. Corneal endothelium is a monolayer of hexagonal cells tightly adherent to one another. In vivo endothelial cells are arrested in G1-phase of cell cycle. The endothelium forms a physiological barrier between the nutrient-rich AqH and the corneal stroma. Tight and gap cell junctions and dynamic pump-leak system maintains corneal deturgescence and permit sufficient nutrient delivery into the stroma and epithelium. Disruption of the endothelial cells results in corneal edema. Modern non-contact real-time imaging of the cornea include specular microscopy, optical coherence tomography and in vivo confocal laser scanning microscopy. These methods can help to visualize corneal layers (during keratorefractive surgery, pre- and postoperative periods), detect localization and etiology of pathological changes.
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Winkler, B. S., M. V. Riley, M. I. Peters, and F. J. Williams. "Chloride is required for fluid transport by the rabbit corneal endothelium." American Journal of Physiology-Cell Physiology 262, no. 5 (May 1, 1992): C1167—C1174. http://dx.doi.org/10.1152/ajpcell.1992.262.5.c1167.

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The role of chloride in fluid transport of the rabbit corneal endothelium was examined by measuring changes in corneal thickness following ion substitutions or addition of ion transport inhibitors in media superfusing the isolated tissue. Normal fluid transport is indicated by maintenance of constant thickness in a fresh cornea or thinning (deturgescence) of a preswollen deepithelialized cornea to its initial thickness at approximately 40 microns/h. These patterns are seen when tissues are superfused with HCO(3-)-Ringer containing 114 mM Cl-. When Cl- was substituted with gluconate, glucuronate, or SO4(2-) fresh and preswollen corneas immediately thinned at greater than 150 microns/h to a value less than 300 microns and then began to swell at 30 microns/h to above their original thickness. Substitution of Cl- with NO3- or Br- had a negligible immediate thinning effect, but fresh corneas subsequently swelled and preswollen corneas failed to deturgesce fully. The rapid thinning (called a "downtransient") observed with gluconate, glucuronate, and SO4(2-) also occurred in these media when ion and fluid transport were completely inhibited with ouabain or stilbenes or by absence of HCO3-, indicating that the thinning results from osmotic gradients induced by ionic reflection coefficients different from that of Cl-. When the downstransient was avoided in deepithelialized corneas by preswelling with the same Cl(-)-free media on both sides of the cornea, corneas maintained a constant but swollen thickness in gluconate and in NO3- or Br- deturgesced slowly and incompletely; ouabain or stilbenes caused further swelling in all media. We conclude that absence of Cl- partially impairs fluid transport, most probably via its role in a Cl(-)-HCO3- exchanger which has been proposed in a recent model of endothelial fluid transport.
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Riley, Michael V., Barry S. Winkler, Catherine A. Starnes, and Margaret I. Peters. "Fluid and ion transport in corneal endothelium: insensitivity to modulators of Na+-K+-2Cl−cotransport." American Journal of Physiology-Cell Physiology 273, no. 5 (November 1, 1997): C1480—C1486. http://dx.doi.org/10.1152/ajpcell.1997.273.5.c1480.

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The role of Na+-K+-2Cl−cotransport in ion and fluid transport of the corneal endothelium was examined by measuring changes in corneal hydration and uptake of86Rb by the endothelial cell layer. Isolated, intact rabbit corneas maintain normal hydration when they are superfused at the endothelial surface with bicarbonate ([Formula: see text])-Ringer solutions as a result of equilibrium between active ion and fluid transport out of the stromal tissue and leak of fluid into stromal tissue from the aqueous humor. Furosemide and bumetanide did not alter this equilibrium when they were added to the superfusion medium. Uptake of86Rb by the endothelium of the incubated cornea was increased 25% by bumetanide, but uptake in the presence of ouabain (70% less than that of controls) was not changed by bumetanide. In Na+-free medium, uptake of 86Rb was reduced by 58%, but it was unchanged in Cl−-free medium. Calyculin A, a protein phosphatase inhibitor and activator of Na+-K+-Cl−cotransport, was without effect on86Rb uptake. Hypertonicity (345 mosmol/kg) increased uptake slightly, whereas hypotonicity (226 mosmol/kg) caused a 33% decrease. Neither of these changes was significantly different when bumetanide was present in the media. It is concluded that Na+-K+-2Cl−cotransporter activity is not exhibited by the in situ corneal endothelium and does not play a role in the ion and fluid transport of this cell layer. Its presence in cultured endothelial cells may reflect the reported importance of this protein in growth, proliferation, and differentiation.
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Parthasarathi, Priyadarshini, Venipriya, Justin Prashanth, and Hannah Ranjee Prasanth. "Atypical presentation of macular corneal dystrophy." Indian Journal of Clinical and Experimental Ophthalmology 8, no. 3 (October 15, 2022): 428–30. http://dx.doi.org/10.18231/j.ijceo.2022.086.

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A 65-year old male patient presented to our ophthalmology OPD for regular check up. On examination visual acuity of the right eye was 6/24 improving to 6/12p with pinhole and left eye was 6/18 improving with pinhole 6/9. On examination of anterior segment both eyes cornea showed multiple white round deposits at deep posterior stroma and Descemet membrane – endothelium complex scattered circumferentially in the peripheral cornea and the central cornea clear and lens showed Immature cataract. Fundus examination was within normal limits. A differential diagnosis of stromal corneal dystrophy or endothelial corneal dystrophy was made. By exclusion, we came to the diagnosis of macular corneal dystrophy.
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Westin, Ida Maria, Andreas Viberg, Berit Byström, and Irina Golovleva. "Lower Fractions of TCF4 Transcripts Spanning over the CTG18.1 Trinucleotide Repeat in Human Corneal Endothelium." Genes 12, no. 12 (December 17, 2021): 2006. http://dx.doi.org/10.3390/genes12122006.

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Fuchs’ endothelial corneal dystrophy (FECD) is a bilateral disease of the cornea caused by gradual loss of corneal endothelial cells. Late-onset FECD is strongly associated with the CTG18.1 trinucleotide repeat expansion in the Transcription Factor 4 gene (TCF4), which forms RNA nuclear foci in corneal endothelial cells. To date, 46 RefSeq transcripts of TCF4 are annotated by the National Center of Biotechnology information (NCBI), however the effect of the CTG18.1 expansion on expression of alternative TCF4 transcripts is not completely understood. To investigate this, we used droplet digital PCR for quantification of TCF4 transcripts spanning over the CTG18.1 and transcripts with transcription start sites immediately downstream of the CTG18.1. TCF4 expression was analysed in corneal endothelium and in whole blood of FECD patients with and without CTG18.1 expansion, in non-FECD controls without CTG18.1 expansion, and in five additional control tissues. Subtle changes in transcription levels in groups of TCF4 transcripts were detected. In corneal endothelium, we found a lower fraction of transcripts spanning over the CTG18.1 tract compared to all other tissues investigated.
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Cerro-Tello, G., S. Benito-Martínez, C. Cacho-Navas, S. Barroso, G. de Rivas-Hidalgo, and J. Millán. "A unique F-actin and junctional organization that maintains the corneal endothelial barrier." IBJ Plus 1, s5 (June 3, 2022): 6. http://dx.doi.org/10.24217/2531-0151.22v1s5.00006.

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Introduction: The corneal endothelium is responsible for the correct hydration of the corneal stroma and for an adequate transport through this tissue. Corneal endothelial layer has a particular organization to maintain its curved shape and function. The corneal endothelium has low proliferative capacity and form a monolayer that is subjected to an even mechanical tension coming from the positive pressure of the aqueous humor. Preserving their barrier function under suboptimal conditions, such as corneal pathologies, age and transplantation, is essential for maintaining corneal transparency. Material and methods: We have investigated the structure and the proteins in charge of maintaining corneal endothelial barrier function by confocal microscopy and time lapse spinning disk microscopy in murine corneas ex vivo, and hepatic organoids. Results: We have characterized a novel filamentous actin network that organizes into radial structures arising from the center of the cell under the nucleus towards cell-cell junctions. This structure is also observed in spherical epithelial organoids whose cells are also exposed to positive luminal pressure. Due to the simplicity of the model, it can be easily implemented in any clinic which leads to increasing ADR and preventing CRC, but requires validation in large multicenter trials.
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Malyugin, B. E., O. P. Antonova, and Z. R. Ebzeeva. "The comorbidity of keratoconus and Fuchs' endothelial corneal dystrophy (clinical cases)." Fyodorov journal of ophthalmic surgery, no. 3 (October 8, 2021): 95–103. http://dx.doi.org/10.25276/0235-4160-2021-3-95-103.

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Purpose. To describe the clinical cases and surgery results in patients with concomitant of keratoconus and Fuchs' corneal endothelial dystrophy. Material and methods. Retrospective analysis of 3 patients using different surgical techniques. All patients were female, they underwent diagnostic procedures including: keratotopography, optical coherence tomography of the anterior segment of the eye, Scheimpflug keratotomography, endothelial microscopy. First patient underwent penetrating keratoplasty (PKP), the second one – descemet stripping automated endothelial keratoplasty (DSEK), and the third one – descemet membrane endothelial keratoplasty (DMEK). Results. In all cases the combination of keratoconus and fuchs endothelial corneal dystrophy occurred in one eye, while cornea guttata was observed in both eyes. The diagnosis of keratoconus was complicated by the presence of corneal edema due to endothelial dysfunction. As a result, visual rehabilitation was achieved in 2 patients after PKP and DSEK, and in the third case (DMEK), the presence of pronounced opacities of the stroma in the central zone did not result in increase of visual acuity, despite the good function of the graft endothelium, which required the PKP. Conclusion. Surgical tactics should be based primary on the replacement of the pathologically altered endothelial monolayer (DSEK, DMEK). As for the simultaneous replacement of the corneal stroma (PKP), the decision is based on the progression of keratoconus, the degree of corneal thinning, and the presence of its surface irregularity. Key words: Fuchs' endothelial corneal dystrophy, keratoconus, endothelial keratoplasty, penetrating keratoplasty, Descemet's membrane endothelial keratoplasty, corneal endothelium
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31

Ahmedov, A. K., T. Z. Kerimov, Kh D. Tonaeva, B. E. Malygin, and S. A. Borzenok. "Technology for obtaining an ultrathin posterior lamellar corneal graft at the Eye Tissue Bank." Russian Journal of Transplantology and Artificial Organs 22, no. 3 (October 6, 2020): 167–73. http://dx.doi.org/10.15825/1995-1191-2020-3-167-173.

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Objective: to develop technologies for preoperative preparation of the posterior lamellar corneal graft based on our own formulation of the preservation medium for optimal dehydration of the donor cornea and a technique for cutting out an ultrathin flap using an optimized method at the Eye Tissue Bank. Materials methods. In a series of experimental studies, we obtained data on the hydration level of cadaveric donor corneas that were preserved in various solutions at different observation periods. Using 16 corneas, analytical weighing and pachymetry were performed via optical coherence tomography in the experimental (n = 8) and control (n = 8) groups. Morphological and functional characteristics of the corneal endothelium were then assessed. At the next stage of work, ultrathin grafts were formed from 16 corneas after hypothermic preservation in the experimental (n = 8) and control (n = 8) solutions by single-pass microkeratome, followed by microscopy of the samples using a scanning electron microscope. Results. After the first days of preservation in the proposed solution, there was dehydration of 9% cornea in the experimental group in comparison with the samples of the control group. After 4 days of preservation, there was no reliable difference found between the groups (p > 0.05) in the study of the endothelial cell viability of ultra-thin corneal grafts by immunofluorescent microscopy using the «Live and dead» marker. Scanning electron microscopy revealed that corneal stromal collagen fibers, preserved in the proposed medium, retained their integrity. Conclusion. The proposed technology can be recommended for use at eye banks for formation of an ultra-thin corneal graft at the preoperative stage.
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Hsueh, Yi-Jen, Yaa-Jyuhn James Meir, Lung-Kun Yeh, Tze-Kai Wang, Chieh-Cheng Huang, Tsai-Te Lu, Chao-Min Cheng, Wei-Chi Wu, and Hung-Chi Chen. "Topical Ascorbic Acid Ameliorates Oxidative Stress-Induced Corneal Endothelial Damage via Suppression of Apoptosis and Autophagic Flux Blockage." Cells 9, no. 4 (April 11, 2020): 943. http://dx.doi.org/10.3390/cells9040943.

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Compromised pumping function of the corneal endothelium, due to loss of endothelial cells, results in corneal edema and subsequent visual problems. Clinically and experimentally, oxidative stress may cause corneal endothelial decompensation after phacoemulsification. Additionally, in vitro and animal studies have demonstrated the protective effects of intraoperative infusion of ascorbic acid (AA). Here, we established a paraquat-induced cell damage model, in which paraquat induced reactive oxygen species (ROS) production and apoptosis in the B4G12 and ARPE-19 cell lines. We demonstrate that oxidative stress triggered autophagic flux blockage in corneal endothelial cells and that addition of AA ameliorated such oxidative damage. We also demonstrate the downregulation of Akt phosphorylation in response to oxidative stress. Pretreatment with ascorbic acid reduced the downregulation of Akt phosphorylation, while inhibition of the PI3K/Akt pathway attenuated the protective effects of AA. Further, we establish an in vivo rabbit model of corneal endothelial damage, in which an intracameral infusion of paraquat caused corneal opacity. Administration of AA via topical application increased its concentration in the corneal stroma and reduced oxidative stress in the corneal endothelium, thereby promoting corneal clarity. Our findings indicate a perioperative strategy of topical AA administration to prevent oxidative stress-induced damage, particularly for those with vulnerable corneal endothelia.
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Li, Shimin, Edward Kim, and Joseph A. Bonanno. "Fluid transport by the cornea endothelium is dependent on buffering lactic acid efflux." American Journal of Physiology-Cell Physiology 311, no. 1 (July 1, 2016): C116—C126. http://dx.doi.org/10.1152/ajpcell.00095.2016.

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Maintenance of corneal hydration is dependent on the active transport properties of the corneal endothelium. We tested the hypothesis that lactic acid efflux, facilitated by buffering, is a component of the endothelial fluid pump. Rabbit corneas were perfused with bicarbonate-rich (BR) or bicarbonate-free (BF) Ringer of varying buffering power, while corneal thickness was measured. Perfusate was collected and analyzed for lactate efflux. In BF with no added HEPES, the maximal corneal swelling rate was 30.0 ± 4.1 μm/h compared with 5.2 ± 0.9 μm/h in BR. Corneal swelling decreased directly with [HEPES], such that with 60 mM HEPES corneas swelled at 7.5 ± 1.6 μm/h. Perfusate [lactate] increased directly with [HEPES]. Similarly, reducing the [HCO3−] increased corneal swelling and decreased lactate efflux. Corneal swelling was inversely related to Ringer buffering power (β), whereas lactate efflux was directly related to β. Ouabain (100 μM) produced maximal swelling and reduction in lactate efflux, whereas carbonic anhydrase inhibition and an monocarboxylic acid transporter 1 inhibitor produced intermediate swelling and decreases in lactate efflux. Conversely, 10 μM adenosine reduced the swelling rate to 4.2 ± 0.8 μm/h and increased lactate efflux by 25%. We found a strong inverse relation between corneal swelling and lactate efflux ( r = 0.98, P < 0.0001). Introducing lactate in the Ringer transiently increased corneal thickness, reaching a steady state (0 ± 0.6 μm/h) within 90 min. We conclude that corneal endothelial function does not have an absolute requirement for bicarbonate; rather it requires a perfusing solution with high buffering power. This facilitates lactic acid efflux, which is directly linked to water efflux, indicating that lactate flux is a component of the corneal endothelial pump.
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Tkachenko, I. S., B. E. Malyugin, S. A. Borzenok, D. S. Ostrovskiy, and S. Y. Kalinnikova. "Experimental rationale for using a viscoprotection of the corneal endothelium on the graft formed with a femtosecond laser for the descemet stripping endothelial keratoplasty." Modern technologies in ophtalmology, no. 2 (June 15, 2021): 94–96. http://dx.doi.org/10.25276/2312-4911-2021-2-94-96.

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Purpose. To rationale experimentally the use of a viscoprotection of the corneal endothelium on the graft formed with a femtosecond laser for the descemet stripping endothelial keratoplasty. Material and methods. In our study, we used 12 pig's corneoscleral discs. The preservation time before the experiment averaged 12±4 hours. The corneas were divided into 2 groups. In the operating room, the graft was formed using an LDV Z8 femtosecond laser (Ziemer, Switzerland) from the endothelial side. Before applanation of the donor cornea and femtolaser head, a 1% solution of hydroxypropyl methylcellulose (HPMC) was applied to the endothelium - experimental group. The control group was appraised according to the standard technique, with the application of a few drops of a solution for storing the corneas. Then the applanation was monitored and evaluated by laser optical coherence tomography. Then the graft was separated from the bed and transferred to a conservation medium. Under laboratory conditions, to determine the viability of endothelial cells, the graft was stained with a «vital» dye with the commercial name Life and Dead (Abcam, UK) and placed in a confocal laser scanning microscope. Endothelial cells were counted using the ImageJ software. Results. In the experimental and control groups, the number of living endothelial cells (EC) was 91.06±1.49% and 83.86±2.14%, respectively (p<0.001). The number of dead ECs in the control group was 7.2±0.65% more than in the experimental group and amounted to 16.14±2.14% and 8.94±1.49%, respectively (p<0.001). Conclusion. The study demonstrated that the use of viscoprotection of the corneal graft endothelium for posterior lamellar keratoplasty is quite effective, and significantly reduces the loss of EC at the stage of cutting out the graft with a femtosecond laser. Key words: descemet stripping endothelial keratoplasty, femtosecond laser, vital dyes.
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Fontes, Bruno Machado, Francisco Bandeira, Ricardo Menon Nosé, and Patrick Frensel Tzelikis. "Essentials of the corneal endothelium for the cataract surgeon." Global Journal of Cataract Surgery and Research in Ophthalmology 1 (September 21, 2022): 64–80. http://dx.doi.org/10.25259/gjcsro_13_2022.

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The human eye is an optical system with two lenses in parallel, with complementary functions essential to vision: the cornea and the lens. There is an intimate relationship between these two structures, especially during cataract surgery when there is inevitably corneal endothelium injury at different severity levels. Every cataract surgeon should be aware of the functioning of the fragile corneal tissue, especially its noblest layer and responsible for corneal transparency: the endothelium. It is of paramount importance to be able to identify the different endothelial pathologies and local conditions associated with greater tissue damage before cataract surgery, as well as to proceed individually in the pre-operative evaluation, during surgery (choice of supplies, technologies and techniques) and prescription of medications or need for additional procedures in the post-operative period. There are several conditions peculiar to cataract surgery and others to the corneal endothelium itself that are described and discussed, as well as information about the physiology, diagnosis and clinical and surgical treatment of diseases that affect it.
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36

Wieben, Eric D., Ross A. Aleff, Tommy A. Rinkoski, Keith H. Baratz, Shubham Basu, Sanjay V. Patel, Leo J. Maguire, and Michael P. Fautsch. "Comparison of TCF4 repeat expansion length in corneal endothelium and leukocytes of patients with Fuchs endothelial corneal dystrophy." PLOS ONE 16, no. 12 (December 2, 2021): e0260837. http://dx.doi.org/10.1371/journal.pone.0260837.

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Expansion of CTG trinucleotide repeats (TNR) in the transcription factor 4 (TCF4) gene is highly associated with Fuchs Endothelial Corneal Dystrophy (FECD). Due to limitations in the availability of DNA from diseased corneal endothelium, sizing of CTG repeats in FECD patients has typically been determined using DNA samples isolated from peripheral blood leukocytes. However, it is non-feasible to extract enough DNA from surgically isolated FECD corneal endothelial tissue to determine repeat length based on current technology. To circumvent this issue, total RNA was isolated from FECD corneal endothelium and sequenced using long-read sequencing. Southern blotting of DNA samples isolated from primary cultures of corneal endothelium from these same affected individuals was also assessed. Both long read sequencing and Southern blot analysis showed significantly longer CTG TNR expansion (>1000 repeats) in the corneal endothelium from FECD patients than those characterized in leukocytes from the same individuals (<90 repeats). Our findings suggest that the TCF4 CTG repeat expansions in the FECD corneal endothelium are much longer than those found in leukocytes.
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37

Pigatto, João A. T., Cristine Cerva, Cesar D. Freire, Fernando C. Abib, Luciano P. Bellini, Paulo S. M. Barros, and José L. Laus. "Morphological analysis of the corneal endothelium in eyes of dogs using specular microscopy." Pesquisa Veterinária Brasileira 28, no. 9 (September 2008): 427–30. http://dx.doi.org/10.1590/s0100-736x2008000900006.

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Both healthy eyes of 10 six-year-old male and female mongrel dogs were studied. With a contact specular microscope the corneal endothelium was examined. Endothelial cells were analyzed in the central and peripheral cornea. Morphological analysis with regard to polymegathism and pleomorphism was performed. Three images of each region with at least 100 cells were obtained. The analysis showed that polygonal cells formed a mosaic-like pattern uniform in size and shape. The predominant number of cells was hexagonal. The polymegathism index was 0.22. The study demonstrates that the morphology of the normal corneal endothelial cells of dogs is similar to that found in the human cornea.
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38

Borzenok, S. A., B. E. Malyugin, D. S. Ostrovskiy, A. K. Ahmedov, K. D. Tonaeva, Y. A. Komakh, and M. K. Khubetsova. "Survival of the posterior lamellar cornea graft keratocytes and endothelial cells cultivated in the modified corneal preservation media." Fyodorov journal of ophthalmic surgery, no. 2 (July 15, 2021): 32–39. http://dx.doi.org/10.25276/0235-4160-2021-2-32-39.

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Purpose. To study the survival of keratocytes and endothelial cells of a human donor cornea storage in the standard and the new media which was specifically designed for optimized cornea hydration. Material and methods. 2D cell cultures of keratocytes and endothelial cells obtained from the Eye tissue bank were used for culture in improved storage media over a period of 14 and 7 days subsequently. To confirm phenotype characteristics, the cells were stained by the following markers: for keratocytes – Lumikan, Keratocan, and α-smooth muscle actin; for endothelial cells – ZO-1 and Na/K-ATPase. The onset of apoptosis in cell culture of keratocytes were detected with Cytochrome C, BAX, and Caspase 3 and 8. Viability of cell cultures after the cultivation was carried out using a commercial set of "Live and Dead". Morphology of the endothelial cells was assessed using an electron scanning microscope. Results. It was shown that the 2D keratocyte culture cultured in the improved storage media expressed specific markers: Lumican, Keratocan, and did not express α-smooth muscle actin. There were no markers of apoptosis in the cell culture of keratocytes after 14 days of cultivation. Corneal endothelium cultured in the improved storage media expresses ZO-1, Na/K-ATPase and presented hexagonal cell shape morphology according to electron microscopy. Conclusion. The improved storage media allow to preserve the unique phenotype of keratocytes, with a slight decrease in proliferative cells activity during 14 days. The media maintain a viable and functional corneal endothelium for at least seven days of cultivation. Key words: cell culture; corneal endothelium; keratocyte; posterior lamellar graft, corneal storage media.
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39

Jovanovic, Vesna, and Ljubisa Nikolic. "Graft stability after endothelial keratoplasty." Vojnosanitetski pregled 72, no. 11 (2015): 989–95. http://dx.doi.org/10.2298/vsp140422100j.

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Bacground/Aim. Techniques for replacing the corneal endothelium have been improved. The host-graft interface is the key to graft adhesion and visual recovery. The aim of this study was to establish graft stability after Descemet stripping with endothelial keratoplasty (DSEK), compare it to the graft stability after endothelial keratoplasty with the intact posterior corneal layers (nDSEK) in the rabbit cornea, and to investigate the nature of wound healing. Methods. Adult white rabbits (n = 20) were divided in two experimental groups: ten rabbits underwent monocular DSEK, and ten rabbits underwent endothelial keratoplasty without Descemet stripping (nDSEK). On the second postoperative day a horizontal dislocation of the graft was tried using the Lindstrom roller in each animal. Corneas were processed for the light microscopy study. Results. Rolling the Lindstrom instrument over the corneal surface did not cause horizontal dislocation in any of the operated eyes. In the DSEK group light microscopy revealed the lack of inflammation and fibrosis at the clearly distinctive donor-recipient interface (DRI). Retrocorneal membrane was found in two eyes. In nDSEK group, the host Descemet` s membrane (DM) was intact without endothelial cells, with good graft apposition, without inflammation, fibrosis, or retrocorneal membrane. Conclusion. This study suggests that there is no difference in graft stability in DSEK compared to nDSEK in rabbit corneas. Wounds healed at DRI by hypocellular scarring only in both experimental groups.
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40

Igarashi, Haruyoshi, Yasunaga Katsuta, Yoshiharu Nakazato, and Tohru Kawasaki. "The Use of an Opacitometer to Compare the In Vitro Cornea Opacifying Effects of Timolol With and Without Benzalkonium Chloride." Alternatives to Laboratory Animals 19, no. 2 (April 1991): 263–70. http://dx.doi.org/10.1177/026119299101900220.

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We have evaluated a new in vitro opacitometer method as an alternative to the in vivo Draize test for ocular irritancy. Several concentrations of timolol maleate (timolol) with or without 0.005% benzalkonium chloride were applied to porcine isolated corneas which were either intact or with the epithelium, endothelium, or both epithelium and endothelium removed. Corneal opacities were measured using an opacitometer. In general, timolol with benzalkonium chloride caused a greater degree of opacity to develop in the cornea than did timolol alone. At the lower concentrations of timolol, the increased opacity probably represented additive effects of the two compounds. However, at the highest concentration of timolol (5 x 10 2M), there was an enhanced opacification in the presence of benzalkonium chloride, which may have been due to an increase in penetration, particularly through the epithelium. Timolol caused a greater degree of opacity to develop in the isolated intact porcine corneas when the drug was applied to the endothelial surface, than when applied to the epithelial surface or to both the epithelial and endothelial surfaces. However, timolol with benzalkonium chloride caused a greater degree of opacity in the intact cornea, when the drug was applied to both surfaces than when it was applied only to the epithelial or the endothelial surface.
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41

Zhang, Yingnan, Xiao Liu, Wei Liang, Douglas C. Dean, Lijun Zhang, and Yongqing Liu. "Expression and Function of ZEB1 in the Cornea." Cells 10, no. 4 (April 16, 2021): 925. http://dx.doi.org/10.3390/cells10040925.

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ZEB1 is an important transcription factor for epithelial to mesenchymal transition (EMT) and in the regulation of cell differentiation and transformation. In the cornea, ZEB1 presents in all three layers: the epithelium, the stroma and the endothelium. Mutations of ZEB1 have been linked to multiple corneal genetic defects, particularly to the corneal dystrophies including keratoconus (KD), Fuchs endothelial corneal dystrophy (FECD), and posterior polymorphous corneal dystrophy (PPCD). Accumulating evidence indicates that dysfunction of ZEB1 may affect corneal stem cell homeostasis, and cause corneal cell apoptosis, stromal fibrosis, angiogenesis, squamous metaplasia. Understanding how ZEB1 regulates the initiation and progression of these disorders will help us in targeting ZEB1 for potential avenues to generate therapeutics to treat various ZEB1-related disorders.
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42

Meng, Jufeng, Ke Xu, Yinyin Qin, Ya Liu, Lin Xu, Shigang Qiao, Jianzhong An, Jianjun Liu, and Zhenhao Zhang. "Tumor Necrosis Factor-Alpha Disrupts Cx43-Mediated Corneal Endothelial Gap Junction Intercellular Communication." Oxidative Medicine and Cellular Longevity 2022 (September 19, 2022): 1–9. http://dx.doi.org/10.1155/2022/4824699.

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Connexin43 (Cx43)-mediated gap junctions are vital in maintaining corneal endothelium homeostasis. Tumor necrosis factor-alpha (TNF-α) is among the most important inflammatory factors which cause corneal endothelial dysfunction in various eye diseases. However, the effect of TNF-α on Cx43-mediated gap junctions of the corneal endothelium remains undefined. In the current research, we determined the effect of TNF-α on gap junction intercellular communication (GJIC) in rabbit corneal endothelium. To evaluate alterations of GJIC, if any, we treated ex vivo cultured rabbit corneal endothelium with different concentrations of TNF-α (2-20 ng/ml). The localization of Cx43 was analyzed by immunostaining, while RT-qPCR and western blot were used to profile the expression of Cx43 and zonula occludens-1 (ZO-1). The association between ZO-1 and Cx43 was evaluated using immunoprecipitation and double staining. GJIC activity was determined by the scrap loading and dye transfer assay (SLDT). Our data demonstrated that a high concentration of TNF-α (10 ng/ml and 20 ng/ml) disrupts the Cx43 mediated gap junction distribution in rabbit corneal endothelium and suppresses the expression of Cx43 protein. Furthermore, rabbit corneal endothelial GJIC was inhibited due to the decreased association between the ZO-1 and Cx43 proteins. Current results demonstrate that TNF-α inhibits corneal endothelial GJIC via decreasing the association between ZO-1 and Cx43, disrupting the distribution of Cx43, and downregulating the expression of Cx43 protein. This study offers a new theoretical foundation for diagnosing and treating corneal endothelial cell decompensation induced by elevated TNF-α in various eye diseases.
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43

Dada, T., R. Gupta, S. I. Tinwala, A. Sobti, and A. Panda. "Repositioning of Ahmed glaucoma valve tube in the anterior chamber with prolene sutures to manage tube-endothelial touch." Nepalese Journal of Ophthalmology 4, no. 2 (July 26, 2012): 309–11. http://dx.doi.org/10.3126/nepjoph.v4i2.6549.

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Background: Corneal endothelial damage is a known complication of aqueous shunt surgery. Objective: To describe a new technique for repositioning the Ahmed glaucoma valve tube in a case of tube-endothelial touch.Case: A patient with advanced glaucoma, having undergone Ahmed glaucoma valve (AVG) implantation, developed localized corneal endothelial damage due to contact between the tube and superior corneal endothelium. Two 10-0 prolene anchor sutures were passed over the tube in the anterior chamber, repositioning it away from the endothelium, thus preventing further damage to the corneal endothelium. Resolution of corneal oedema was noted without affecting the tube drainage and intraocular pressure. Conclusion: Intracameral repositioning of the shunt tube using prolene sutures is a useful technique for correcting the tube malposition.DOI: http://dx.doi.org/10.3126/nepjoph.v4i2.6549 Nepal J Ophthalmol 2012; 4 (2): 309-411
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44

Ong, Hon Shing, Gary Peh, Dawn Jin Hui Neo, Heng-Pei Ang, Khadijah Adnan, Chan Lwin Nyein, Fernando Morales-Wong, Maninder Bhogal, Viridiana Kocaba, and Jodhbir S. Mehta. "A Novel Approach of Harvesting Viable Single Cells from Donor Corneal Endothelium for Cell-Injection Therapy." Cells 9, no. 6 (June 9, 2020): 1428. http://dx.doi.org/10.3390/cells9061428.

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Donor corneas with low endothelial cell densities (ECD) are deemed unsuitable for corneal endothelial transplantation. This study evaluated a two-step incubation and dissociation harvesting approach to isolate single corneal endothelial cells (CECs) from donor corneas for corneal endothelial cell-injection (CE-CI) therapy. To isolate CECs directly from donor corneas, optimization studies were performed where donor Descemet’s membrane/corneal endothelium (DM/CE) were peeled and incubated in either M4-F99 or M5-Endo media before enzymatic digestion. Morphometric analyses were performed on the isolated single cells. The functional capacities of these cells, isolated using the optimized simple non-cultured endothelial cells (SNEC) harvesting technique, for CE-CI therapy were investigated using a rabbit bullous keratopathy model. The two control groups were the positive controls, where rabbits received cultured CECs, and the negative controls, where rabbits received no CECs. Whilst it took longer for CECs to dislodge as single cells following donor DM/CE incubation in M5-Endo medium, CECs harvested were morphologically more homogenous and smaller compared to CECs obtained from DM/CE incubated in M4-F99 medium (p < 0.05). M5-Endo medium was hence selected as the DM/CE incubation medium prior to enzymatic digestion to harvest CECs for the in vivo cell-injection studies. Following SNEC injection, mean central corneal thickness (CCT) of rabbits increased to 802.9 ± 147.8 μm on day 1, gradually thinned, and remained clear with a CCT of 385.5 ± 38.6 μm at week 3. Recovery of corneas was comparable to rabbits receiving cultured CE-CI (p = 0.40, p = 0.17, and p = 0.08 at weeks 1, 2, and 3, respectively). Corneas that did not receive any cells remained significantly thicker compared to both SNEC injection and cultured CE-CI groups (p < 0.05). This study concluded that direct harvesting of single CECs from donor corneas for SNEC injection allows the utilization of donor corneas unsuitable for conventional endothelial transplantation.
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45

Varkoly, Gréta, Tibor G. Hortobágyi, Enikő Gebri, János Bencze, Tibor Hortobágyi, and László Módis. "Expression Pattern of Tenascin-C, Matrilin-2, and Aggrecan in Diseases Affecting the Corneal Endothelium." Journal of Clinical Medicine 11, no. 20 (October 11, 2022): 5991. http://dx.doi.org/10.3390/jcm11205991.

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Purpose: The aim of this study was to examine the expression pattern of tenascin-C, matrilin-2, and aggrecan in irreversible corneal endothelial pathology such as pseudophakic bullous keratopathy (PBK) and Fuchs’ endothelial corneal dystrophy (FECD), which most frequently require corneal transplantation. Materials and methods: Histological specimens of corneal buttons removed during keratoplasty were investigated in PBK (n = 20) and FECD (n = 9) and compared to healthy control corneas (n = 10). The sections were studied by chromogenic immunohistochemistry (CHR-IHC) and submitted for evaluation by two investigators. Semiquantitative scoring (0 to 3+) was applied according to standardized methods at high magnification (400x). Each layer of the cornea was investigated; in addition, the stroma was subdivided into anterior, middle, and posterior parts for more precise analysis. In case of non-parametric distribution Mann–Whitney test was applied to compare two groups. Kruskal–Wallis and Dunn’s multiple comparisons tests have been applied for comparison of the chromogenic IHC signal intensity among corneal layers within the control and patient groups. Differences of p < 0.05 were considered as significant. Results: Significantly elevated tenascin-C immunopositivity was present in the epithelium and every layer of the stroma in both pathologic conditions as compared to normal controls. In addition, also significantly stronger matrilin-2 positivity was detected in the epithelium; however, weaker reaction was present in the endothelium in PBK cases. Minimal, but significantly elevated immunopositivity could be observed in the anterior and posterior stroma in the FECD group. Additionally, minimally, but significantly higher aggrecan immunoreaction was present in the anterior stroma in PBK and in the posterior stroma in both endothelial disorders. All three antibodies disclosed the strongest reaction in the posterior stroma either in PBK or in FECD cases. Conclusions: These extracellular matrix molecules disclosed up to moderate immunopositivity in the corneal layers in varying extents. Through their networking, bridging, and adhesive abilities these proteins are involved in corneal regeneration and tissue reorganization in endothelial dysfunction.
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46

Reneker, L. W., D. W. Silversides, L. Xu, and P. A. Overbeek. "Formation of corneal endothelium is essential for anterior segment development - a transgenic mouse model of anterior segment dysgenesis." Development 127, no. 3 (February 1, 2000): 533–42. http://dx.doi.org/10.1242/dev.127.3.533.

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The anterior segment of the vertebrate eye is constructed by proper spatial development of cells derived from the surface ectoderm, which become corneal epithelium and lens, neuroectoderm (posterior iris and ciliary body) and cranial neural crest (corneal stroma, corneal endothelium and anterior iris). Although coordinated interactions between these different cell types are presumed to be essential for proper spatial positioning and differentiation, the requisite intercellular signals remain undefined. We have generated transgenic mice that express either transforming growth factor (alpha) (TGF(alpha)) or epidermal growth factor (EGF) in the ocular lens using the mouse (alpha)A-crystallin promoter. Expression of either growth factor alters the normal developmental fate of the innermost corneal mesenchymal cells so that these cells often fail to differentiate into corneal endothelial cells. Both sets of transgenic mice subsequently manifest multiple anterior segment defects, including attachment of the iris and lens to the cornea, a reduction in the thickness of the corneal epithelium, corneal opacity, and modest disorganization in the corneal stroma. Our data suggest that formation of a corneal endothelium during early ocular morphogenesis is required to prevent attachment of the lens and iris to the corneal stroma, therefore permitting the normal formation of the anterior segment.
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47

Gupta, Kishan, and Sophie X. Deng. "Corneal Endothelial Decompensation." Klinische Monatsblätter für Augenheilkunde 237, no. 06 (June 2020): 745–53. http://dx.doi.org/10.1055/a-1128-4445.

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AbstractEndothelial decompensation can occur from a variety of insults to the endothelium that result in loss of stromal clarity. Direct insults to the endothelium commonly occur in inherited, inflammatory, traumatic, immunological, and infectious etiologies. These injuries may cause transient injury without decompensation, but repetitive injury or severe isolated injury can lead to permanent non-compensatory endothelial cell loss. Elevated intraocular pressure can induce stromal hydration, either primarily or secondarily. With partial and full thickness corneal transplants, chronic endothelial dysfunction can be treated surgically when medical therapy proves inadequate. Practitioners should be aware of the underlying causes for corneal endothelial injury.
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48

Igarashi, Haruyoshi, Yasumaja Katsuta, Hidefumi Matsuno, Yoshiharu Nakazato, and Tohru Kawasaki. "Carbachol HCl-Induced Opacity of Porcine Isolated Cornea." Alternatives to Laboratory Animals 16, no. 4 (June 1989): 322–30. http://dx.doi.org/10.1177/026119298901600403.

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The in vitro development of porcine corneal opacity induced by carbachol was monitored using a simple, specially constructed opacitometer. Corneas were used intact, without epithelium, or without endothelium, or stroma only. Solutions of carbachol were applied to both surfaces, to the epithelial surface only or to the endothelial surface only. When carbachol was applied either to both surfaces or to the epithelial surface only, there was a significant increase in opacity compared with controls in the order: both epithelium and endothelium removed>epithelium removed>endothelium removed>intact. However, when applied to the endothelial surface only of intact and endothelium-removed corneas, carbachol caused an opacity comparable to control values. This confirms that the drug is safe for use as a topical application in the eye. However, the opacity which develops in corneas in response to benzalkonium chloride indicates that great care must be taken in determining the optimal concentration to use as a “wetting agent”.
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49

Alafaleq, Munirah, Cristina Georgeon, Kate Grieve, and Vincent M. Borderie. "Multimodal imaging of pre-Descemet corneal dystrophy." European Journal of Ophthalmology 30, no. 5 (July 12, 2019): 908–16. http://dx.doi.org/10.1177/1120672119862505.

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Purpose: The aim of this study was to assess structural and histological changes associated with pre-Descemet corneal dystrophy with multimodal in vivo imaging. Methods: Retrospective case series including eight corneas from four unrelated male patients with pre-Descemet corneal dystrophy characterized by the presence of punctiform gray opacities located just anterior to the Descemet membrane at slit-lamp examination of both eyes. In vivo confocal microscopy images were obtained in the central, paracentral, and peripheral corneal zones from the superficial epithelial cell layer down to the corneal endothelium in both eyes. Spectral domain optical coherence tomography scans (central and limbal zones) and mapping of both corneas were acquired. Results: Diffuse small extracellular stromal deposits, presence of enlarged hyperreflective keratocytes in the posterior stroma with either hyperreflective or hyporeflective intracellular dots, and presence of activated keratocytes in the very anterior stroma were observed in all corneas with in vivo confocal microscopy. Spectral domain optical coherence tomography scans showed a hyperreflective line anterior to Descemet’s membrane running from limbus to limbus and associated with a second thinner hyperreflective line just beneath Bowman’s layer. Fine hyperreflective particles were observed in the posterior, mid, and anterior stroma on optical coherence tomography scans. Conclusion: The clinical presentation and structural anomalies found in isolated sporadic pre-Descemet corneal dystrophy are in favor of a degenerative process affecting corneal keratocytes with no epithelial or endothelial involvement. The maximum damage is found just anterior to the Descemet membrane resulting in pre-Descemet membrane location of stromal opacities. Multimodal imaging of cornea reveals that the disorder affects the whole stroma and it permits better understanding of pre-Descemet corneal dystrophy pathophysiology together with ascertained diagnosis.
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50

Silva, Vanessa Ruiz Moura da, Maria Cristina Caldart de Andrade, Claudia Skilhan Faganello, Marcela Torikachvili, Andre Silva Carissimi, and João Antonio Tadeu Pigatto. "Evaluation of equine corneal endothelium after exposure to 0.5% indocyanine green - in vitro study." Semina: Ciências Agrárias 39, no. 2 (March 15, 2018): 613. http://dx.doi.org/10.5433/1679-0359.2018v39n2p613.

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The purpose of the study was to investigate whether indocyanine green (ICG) dye damages the corneal endothelium of horses. Twenty-four corneas of 12 healthy equines, males or females, of different ages were used in this study. Only eyes with no ocular findings were used. Randomly, one eye was included in the treatment group and one in the control group. The eyes of the treatment group were exposed for 1 minute to dye ICG 0.5%. After that the endothelium of all eyes was stained with trypan blue and alizarin red S and analyzed and photographed under an optical microscope. Areas with damaged endothelial cells were manually measured and quantified using software for morphometric analysis and expressed as a percentage of cell damage. In all eyes examined areas of cell damage were observed in both corneas of the control group and the treatment group. The mean endothelial damage was 0.8 ± 0.37% in the treatment group and 0.97 ± 0.39% in the control. The Qui-square test stated that treatment and control group were not different. The ICG 0.5% did not cause acute damage to equine corneal endothelium.
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