Journal articles: 'Retinal vascular remodeling'

1

Ricard, Nicolas, Delphine Ciais, Sandrine Levet, Mariela Subileau, Christine Mallet, Teresa A. Zimmers, Se-Jin Lee, Marie Bidart, Jean-Jacques Feige, and Sabine Bailly. "BMP9 and BMP10 are critical for postnatal retinal vascular remodeling." Blood 119, no. 25 (June 21, 2012): 6162–71. http://dx.doi.org/10.1182/blood-2012-01-407593.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Abstract ALK1 is a type I receptor of the TGF-β family that is involved in angiogenesis. Circulating BMP9 was identified as a specific ligand for ALK1 inducing vascular quiescence. In this work, we found that blocking BMP9 with a neutralizing antibody in newborn mice significantly increased retinal vascular density. Surprisingly, Bmp9-KO mice did not show any defect in retinal vascularization. However, injection of the extracellular domain of ALK1 impaired retinal vascularization in Bmp9-KO mice, implicating another ligand for ALK1. Interestingly, we detected a high level of circulating BMP10 in WT and Bmp9-KO pups. Further, we found that injection of a neutralizing anti-BMP10 antibody to Bmp9-KO pups reduced retinal vascular expansion and increased vascular density, whereas injection of this antibody to WT pups did not affect the retinal vasculature. These data suggested that BMP9 and BMP10 are important in postnatal vascular remodeling of the retina and that BMP10 can substitute for BMP9. In vitro stimulation of endothelial cells by BMP9 and BMP10 increased the expression of genes involved in the Notch signaling pathway (Jagged1, Dll4, Hey1, Hey2, Hes1) and decreased apelin expression, suggesting a possible cross-talk between these pathways and the BMP pathway.

2

VUGLER, ANTHONY A., MA'AYAN SEMO, ANNA JOSEPH, and GLEN JEFFERY. "Survival and remodeling of melanopsin cells during retinal dystrophy." Visual Neuroscience 25, no. 2 (March 2008): 125–38. http://dx.doi.org/10.1017/s0952523808080309.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

AbstractThe melanopsin positive, intrinsically photosensitive retinal ganglion cells (ipRGCs) of the inner retina have been shown to send wide-ranging projections throughout the brain. To investigate the response of this important cell type during retinal dystrophy, we use the Royal College of Surgeons (RCS) dystrophic rat, a major model of retinal degeneration. We find that ipRGCs exhibit a distinctive molecular profile that remains unaltered during early stages of outer retinal pathology (15 weeks of age). In particular, these cells express βIII tubulin, α-acetylated tubulin, and microtubule-associated proteins (MAPs), while remaining negative for other RGC markers such as neurofilaments, calretinin, and parvalbumin. By 14 months of age, melanopsin positive fibers invade ectopic locations in the dystrophic retina and ipRGC axons/dendrites become distorted (a process that may involve vascular remodeling). The morphological abnormalities in melanopsin processes are associated with elevated immunoreactivity for MAP1b and a reduction in α-acetylated tubulin. Quantification of ipRGCs in whole mounts reveals reduced melanopsin cell number with increasing age. Focusing on the retinal periphery, we find a significant decline in melanopsin cell density contrasted by a stability of melanopsin positive processes. In addition to these findings, we describe for the first time, a distinct plexus of melanopsin processes in the far peripheral retina, a structure that is coincident with a short wavelength opsin cone-enriched rim. We conclude that some ipRGCs are lost in RCS dystrophic rats as the disease progresses and that this loss may involve vascular remodeling. However, a significant number of melanopsin positive cells survive into advanced stages of retinal degeneration and show indications of remodeling in response to pathology. Our findings underline the importance of early intervention in human retinal disease in order to preserve integrity of the inner retinal photoreceptive network.

3

Touyz, Rhian M. "Vascular Remodeling, Retinal Arteries, and Hypertension." Hypertension 50, no. 4 (October 2007): 603–4. http://dx.doi.org/10.1161/hypertensionaha.107.095638.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

García-Ayuso, Diego, Johnny Di Pierdomenico, Manuel Vidal-Sanz, and María P. Villegas-Pérez. "Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration." International Journal of Molecular Sciences 20, no. 18 (September 19, 2019): 4649. http://dx.doi.org/10.3390/ijms20184649.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Inherited or acquired photoreceptor degenerations, one of the leading causes of irreversible blindness in the world, are a group of retinal disorders that initially affect rods and cones, situated in the outer retina. For many years it was assumed that these diseases did not spread to the inner retina. However, it is now known that photoreceptor loss leads to an unavoidable chain of events that cause neurovascular changes in the retina including migration of retinal pigment epithelium cells, formation of “subretinal vascular complexes”, vessel displacement, retinal ganglion cell (RGC) axonal strangulation by retinal vessels, axonal transport alteration and, ultimately, RGC death. These events are common to all photoreceptor degenerations regardless of the initial trigger and thus threaten the outcome of photoreceptor substitution as a therapeutic approach, because with a degenerating inner retina, the photoreceptor signal will not reach the brain. In conclusion, therapies should be applied early in the course of photoreceptor degeneration, before the remodeling process reaches the inner retina.

5

Benn, Andreas, Florian Alonso, Jo Mangelschots, Elisabeth Génot, Marleen Lox, and An Zwijsen. "BMP-SMAD1/5 Signaling Regulates Retinal Vascular Development." Biomolecules 10, no. 3 (March 23, 2020): 488. http://dx.doi.org/10.3390/biom10030488.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Vascular development is an orchestrated process of vessel formation from pre-existing vessels via sprouting and intussusceptive angiogenesis as well as vascular remodeling to generate the mature vasculature. Bone morphogenetic protein (BMP) signaling via intracellular SMAD1 and SMAD5 effectors regulates sprouting angiogenesis in the early mouse embryo, but its role in other processes of vascular development and in other vascular beds remains incompletely understood. Here, we investigate the function of SMAD1/5 during early postnatal retinal vascular development using inducible, endothelium-specific deletion of Smad1 and Smad5. We observe the formation of arterial-venous malformations in areas with high blood flow, and fewer and less functional tip cells at the angiogenic front. The vascular plexus region is remarkably hyperdense and this is associated with reduced vessel regression and aberrant vascular loop formation. Taken together, our results highlight important functions of SMAD1/5 during vessel formation and remodeling in the early postnatal retina.

6

Yu, Dao-Yi, Valerie A. Alder, Stephen J. Cringle, Er-Ning Su, and Margaret Burns. "Intraretinal oxygen distribution in urethan-induced retinopathy in rats." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 6 (June 1, 1998): H2009—H2017. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h2009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

This study was performed to explore the interaction between chronic neural degeneration and the subsequent vascular remodeling. Weekly urethan administration in rats from birth produces a retinopathy model characterized by photoreceptor degeneration, retinal vascular regression, and retinal pigment epithelium (RPE) neovascularization. We investigated the hypothesis that altered oxygen distribution across the retina and choroid could be involved in the vascular changes seen in this retinopathy. We compared measurements of vitreal, intraretinal, and choroidal oxygen tension ([Formula: see text]) distribution in anesthetized and ventilated control and urethan-treated rats at 8 and 16 wk of age with the use of oxygen-sensitive microelectrodes. Striking differences were observed in both choroidal and intraretinal [Formula: see text]distribution in urethan-treated rats compared with controls. At both ages, intrachoroidal [Formula: see text] was much lower in the urethan-treated rats. In addition, the intraretinal[Formula: see text] distribution across the inner retinal layers was more uniform than normal. A small elevation in[Formula: see text] was present at 8 wk in the inner nuclear layer where subsequent vascular regression occurred, and a small reduction in [Formula: see text] was present at the RPE, which recovered to normal values by 16 wk in regions where RPE vessel networks were first evident. Although the retinal arteries were considerably thinner at both ages in the urethan-treated rats, the vitreal [Formula: see text] profiles and superficial retinal [Formula: see text] remained normal. The unexpected and large reduction in the oxygen delivery from the choroid found in the urethan-treated rats may account for the lack of major hyperoxia within the pathological retina and the lower oxygen tension in the RPE before the vascular proliferation in this region. We propose that tissue [Formula: see text] is an important determinant of the vascular remodeling, which is seen in this model of neural degeneration and that the [Formula: see text]distribution changes described in this study help provide a new view of the pathogenesis of this model.

7

Yan, Qi, E. Helene Sage, and Anita E. Hendrickson. "SPARC Is Expressed by Ganglion Cells and Astrocytes in Bovine Retina." Journal of Histochemistry & Cytochemistry 46, no. 1 (January 1998): 3–10. http://dx.doi.org/10.1177/002215549804600102.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

SPARC (secreted protein, acidic and rich in cysteine)/osteonectin is a matricellular, counteradhesive glycoprotein that disrupts cell-matrix interactions, interacts with growth factors and components of extracellular matrix, and modulates the cell cycle, but appears to subserve only minor structural roles. SPARC is expressed in a variety of tissues during embryogenesis and remodeling and is believed to regulate vascular morphogenesis and cellular differentiation. Although usually limited in normal adult tissues, SPARC is expressed at significant levels in the adult central nervous system. Using a monoclonal antibody against bovine bone osteonectin, we have determined the localization of SPARC in newborn (3-day-old) and adult (4–8-year-old) normal bovine retinas. SPARC was present in the soma of ganglion cells and strong reactivity was found in ganglion cell axons. Muller cells displayed no immunoreactivity, but SPARC was present in retinal astrocytes that were identified by the astrocyte marker glial fibrillary acidic protein (GFAP). Newborn calf retina showed a staining pattern similar to that of adult retina but exhibited significantly reduced levels of SPARC. Minimal levels of SPARC protein were also detected in some capillaries of the inner retina of both newborn and adult animals, whereas large vessels were negative. The presence of SPARC in the retina was confirmed by Western blotting of retinal extracts. These data indicate that SPARC originating from both neurons and glia of the inner retina may be an important modulator of retinal angiogenesis. The increased expression of SPARC in adult relative to newborn retinal tissue also indicates that SPARC has an ongoing role in the maintainance of retinal functions.

8

Huang, Hu. "Pericyte-Endothelial Interactions in the Retinal Microvasculature." International Journal of Molecular Sciences 21, no. 19 (October 8, 2020): 7413. http://dx.doi.org/10.3390/ijms21197413.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Retinal microvasculature is crucial for the visual function of the neural retina. Pericytes and endothelial cells (ECs) are the two main cellular constituents in the retinal microvessels. Formation, maturation, and stabilization of the micro-vasculatures require pericyte-endothelial interactions, which are perturbed in many retinal vascular disorders, such as retinopathy of prematurity, retinal vein occlusion, and diabetic retinopathy. Understanding the cellular and molecular mechanisms of pericyte-endothelial interaction and perturbation can facilitate the design of therapeutic intervention for the prevention and treatment of retinal vascular disorders. Pericyte-endothelial interactions are indispensable for the integrity and functionality of retinal neurovascular unit (NVU), including vascular cells, retinal neurons, and glial cells. The essential autocrine and paracrine signaling pathways, such as Vascular endothelial growth factor (VEGF), Platelet-derived growth factor subunit B (PDGFB), Notch, Angipointein, Norrin, and Transforming growth factor-beta (TGF-β), have been well characterized for the regulation of pericyte-endothelial interactions in the neo-vessel formation processes (vasculogenesis and angiogenesis) during embryonic development. They also play a vital role in stabilizing and remodeling mature vasculature under pathological conditions. Awry signals, aberrant metabolisms, and pathological conditions, such as oxidative stress and inflammation, can disrupt the communication between pericytes and endothelial cells, thereby resulting in the breakdown of the blood-retinal barrier (BRB) and other microangiopathies. The emerging evidence supports extracellular exosomes’ roles in the (mis)communications between the two cell types. This review summarizes the essential knowledge and updates about new advancements in pericyte-EC interaction and communication, emphasizing the retinal microvasculature.

9

Habibi-Kavashkohie, Mohammad Reza, Tatiana Scorza, and Malika Oubaha. "Senescent Cells: Dual Implications on the Retinal Vascular System." Cells 12, no. 19 (September 23, 2023): 2341. http://dx.doi.org/10.3390/cells12192341.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Cellular senescence, a state of permanent cell cycle arrest in response to endogenous and exogenous stimuli, triggers a series of gradual alterations in structure, metabolism, and function, as well as inflammatory gene expression that nurtures a low-grade proinflammatory milieu in human tissue. A growing body of evidence indicates an accumulation of senescent neurons and blood vessels in response to stress and aging in the retina. Prolonged accumulation of senescent cells and long-term activation of stress signaling responses may lead to multiple chronic diseases, tissue dysfunction, and age-related pathologies by exposing neighboring cells to the heightened pathological senescence-associated secretory phenotype (SASP). However, the ultimate impacts of cellular senescence on the retinal vasculopathies and retinal vascular development remain ill-defined. In this review, we first summarize the molecular players and fundamental mechanisms driving cellular senescence, as well as the beneficial implications of senescent cells in driving vital physiological processes such as embryogenesis, wound healing, and tissue regeneration. Then, the dual implications of senescent cells on the growth, hemostasis, and remodeling of retinal blood vessels are described to document how senescent cells contribute to both retinal vascular development and the severity of proliferative retinopathies. Finally, we discuss the two main senotherapeutic strategies—senolytics and senomorphics—that are being considered to safely interfere with the detrimental effects of cellular senescence.

10

Задорожний, Олег, Андрій Король, Ілля Насінник, Тарас Кустрін, Володимир Науменко, and Наталія Пасєчнікова. "Precise in vivo adaptive optics imaging of retinal vessels." Oftalmologicheskii Zhurnal, no. 2 (April 25, 2023): 31–38. http://dx.doi.org/10.31288/oftalmolzh202323138.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Adaptive optics (AO) provides new, unique opportunities for in vivo visualization of retinal vasculature. AO retinal vessel imaging can be utilized as a component of multimodal imaging tools to complement conventional diagnostic imaging modalities. Non-invasive and highly promising AO imaging of fundus structures allows the qualitative and quantitative assessment of early signs of retinal vascular remodeling associated with age, arterial hypertension, diabetes mellitus and other disorders.

11

Sharma, Deepti, Geetika Kaur, Shivantika Bisen, Anamika Sharma, Ahmed S. Ibrahim, and Nikhlesh K. Singh. "IL-33 via PKCμ/PRKD1 Mediated α-Catenin Phosphorylation Regulates Endothelial Cell-Barrier Integrity and Ischemia-Induced Vascular Leakage." Cells 12, no. 5 (February 23, 2023): 703. http://dx.doi.org/10.3390/cells12050703.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Angiogenesis, neovascularization, and vascular remodeling are highly dynamic processes, where endothelial cell–cell adhesion within the vessel wall controls a range of physiological processes, such as growth, integrity, and barrier function. The cadherin–catenin adhesion complex is a key contributor to inner blood–retinal barrier (iBRB) integrity and dynamic cell movements. However, the pre-eminent role of cadherins and their associated catenins in iBRB structure and function is not fully understood. Using a murine model of oxygen-induced retinopathy (OIR) and human retinal microvascular endothelial cells (HRMVECs), we try to understand the significance of IL-33 on retinal endothelial barrier disruption, leading to abnormal angiogenesis and enhanced vascular permeability. Using electric cell-substrate impedance sensing (ECIS) analysis and FITC-dextran permeability assay, we observed that IL-33 at a 20 ng/mL concentration induced endothelial-barrier disruption in HRMVECs. The adherens junction (AJs) proteins play a prominent role in the selective diffusion of molecules from the blood to the retina and in maintaining retinal homeostasis. Therefore, we looked for the involvement of adherens junction proteins in IL-33-mediated endothelial dysfunction. We observed that IL-33 induces α-catenin phosphorylation at serine/threonine (Ser/Thr) residues in HRMVECs. Furthermore, mass-spectroscopy (MS) analysis revealed that IL-33 induces the phosphorylation of α-catenin at Thr654 residue in HRMVECs. We also observed that PKCμ/PRKD1-p38 MAPK signaling regulates IL-33-induced α-catenin phosphorylation and retinal endothelial cell-barrier integrity. Our OIR studies revealed that genetic deletion of IL-33 resulted in reduced vascular leakage in the hypoxic retina. We also observed that the genetic deletion of IL-33 reduced OIR-induced PKCμ/PRKD1-p38 MAPK-α-catenin signaling in the hypoxic retina. Therefore, we conclude that IL-33-induced PKCμ/PRKD1-p38 MAPK-α-catenin signaling plays a significant role in endothelial permeability and iBRB integrity.

12

Holden, Joseph M., Sara Al Hussein Al Awamlh, Louis-Philippe Croteau, Andrew M. Boal, Tonia S. Rex, Michael L. Risner, David J. Calkins, and Lauren K. Wareham. "Dysfunctional cGMP Signaling Leads to Age-Related Retinal Vascular Alterations and Astrocyte Remodeling in Mice." International Journal of Molecular Sciences 23, no. 6 (March 12, 2022): 3066. http://dx.doi.org/10.3390/ijms23063066.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

The nitric oxide–guanylyl cyclase-1–cyclic guanylate monophosphate (NO–GC-1–cGMP) pathway is integral to the control of vascular tone and morphology. Mice lacking the alpha catalytic domain of guanylate cyclase (GC1−/−) develop retinal ganglion cell (RGC) degeneration with age, with only modest fluctuations in intraocular pressure (IOP). Increasing the bioavailability of cGMP in GC1−/− mice prevents neurodegeneration independently of IOP, suggesting alternative mechanisms of retinal neurodegeneration. In continuation to these studies, we explored the hypothesis that dysfunctional cGMP signaling leads to changes in the neurovascular unit that may contribute to RGC degeneration. We assessed retinal vasculature and astrocyte morphology in young and aged GC1−/− and wild type mice. GC1−/− mice exhibit increased peripheral retinal vessel dilation and shorter retinal vessel branching with increasing age compared to Wt mice. Astrocyte cell morphology is aberrant, and glial fibrillary acidic protein (GFAP) density is increased in young and aged GC1−/− mice, with areas of dense astrocyte matting around blood vessels. Our results suggest that proper cGMP signaling is essential to retinal vessel morphology with increasing age. Vascular changed are preceded by alterations in astrocyte morphology which may together contribute to retinal neurodegeneration and loss of visual acuity observed in GC1−/− mice.

13

Lobov, Ivan, and Natalia Mikhailova. "The Role of Dll4/Notch Signaling in Normal and Pathological Ocular Angiogenesis: Dll4 Controls Blood Vessel Sprouting and Vessel Remodeling in Normal and Pathological Conditions." Journal of Ophthalmology 2018 (July 5, 2018): 1–8. http://dx.doi.org/10.1155/2018/3565292.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Background. Retina is the highest oxygen-demanding and vascularized tissue in the body. Retinal development and function require proper vascularization and blood vessel function and integrity. Dll4 is most prominently expressed in the endothelium of angiogenic blood vessels and in quiescent arteries and capillaries in all tissues and organs of the mammalian species, and it is the key regulator of blood vessel sprouting.Results. Dll4 is a transmembrane protein that acts as a ligand for Notch receptors 1 and 4. Genetic deletion of Dll4 causes severe abnormalities in embryonic and postnatal vascular development. Deletion of even a single Dll4 allele results in almost complete embryonic lethality due to severe vascular abnormalities, the phenomenon called haploinsufficiency indicating the critical role of Dll4/Notch in vascular development. Dll4/Notch pathway interplays at multiple levels with other signaling pathways including VEGF, Wnt/Fzd, and genes controlling vascular toning. Multiple studies of the effects of Dll4 inhibition were performed in the developing retina to elucidate the key functions of Dll4 in normal and pathological angiogenesis. Several genetic approaches and therapeutic molecules were tested to evaluate the biological and therapeutic effects of acute and prolonged Dll4 inhibition in the eye and oncology.Conclusions. All current studies demonstrated that Dll4 controls blood vessel sprouting, growth, and remodeling in normal and pathological conditions as well as arterial-venous differentiation. Genetic and therapeutic Dll4 modulation studies show that Dll4 inhibition can promote blood vessel sprouting and might be useful to stimulate vessel growth in the ischemic retina and Dll4 is the key modulator of the postangiogenic vascular remodeling that ultimately defines vascular patterning.

14

Lobov, Ivan B., Eunice Cheung, Rajeev Wudali, Jingtai Cao, Gabor Halasz, Yi Wei, Aris Economides, et al. "The Dll4/Notch pathway controls postangiogenic blood vessel remodeling and regression by modulating vasoconstriction and blood flow." Blood 117, no. 24 (June 16, 2011): 6728–37. http://dx.doi.org/10.1182/blood-2010-08-302067.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Abstract Blood vessel remodeling is crucial to the formation of the definitive vasculature, but little is known about the mechanisms controlling this process. We show that Delta-like ligand 4 (Dll4)/Notch pathway regulates vessel regression in normal pathologic conditions. Genetic and pharmacologic inhibition of Dll4/Notch prevented retinal capillary regression in the oxygen-induced retinopathy (OIR) model and during normal development. Deletion of the Notch-regulated ankyrin repeat protein, a negative regulator of the Notch pathway, produced an opposite phenotype. Inhibition of Dll4/Notch reduced vessel occlusion, maintaining blood flow that is essential for survival of microvessels. Dll4/Notch inhibition up-regulated the expression of vasodilators adrenomedullin and suppressed the expression of vasoconstrictor angiotensinogen. Angiotensin II induced rapid nonperfusion and regression of developing retinal capillaries, whereas Ace1 and AT1 inhibitors and adrenomedullin attenuated vasoobliteration in OIR, indicating that both pathways are involved in modulating vessel remodeling. In contrast, inhibition of vascular endothelial growth factor-A (VEGF-A) did not result in a pervasive loss of retinal capillaries, demonstrating that reduced expression of VEGF-A is not the proximate cause of capillary regression in OIR. Modulation of VEGF-A and DII4/Notch signaling produced distinct changes in blood vessel morphology and gene expression, indicating that these pathways can have largely independent functions in vascular remodeling.

15

Erol, Muhammet Kazim, Birumut Gedik, Yigit Caglar Bozdogan, Rojbin Ekinci, Mehmet Bulut, Berna Dogan, Elcin Suren, and Melih Akidan. "Evaluation of Optic Disc, Retinal Vascular Structures, and Acircularity Index in Patients with Idiopathic Macular Telangiectasia Type 2." Diagnostics 13, no. 19 (September 25, 2023): 3046. http://dx.doi.org/10.3390/diagnostics13193046.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Background: We aimed to compare the retinal, optic disc vascular density (ODVD) values, and acircularity index (AI) of patients with idiopathic macular telangiectasia type 2 (IMT) and healthy individuals using the optical coherence tomography angiography (OCTA) device. Methods: The study included 39 patients with IMT and 37 healthy controls. The OCTA findings of the patients and controls were examined. Results: The total, parafoveal and perifoveal vascular density of the superficial capillary plexus, choriocapillaris blood flow, inside-disc ODVD, retinal nerve fiber layer (RNFL), and retinal thicknesses were found to be statistically significantly lower, and the foveal avascular zone value was statistically significantly higher in the IMT group compared to the control group (p = 0.001, p = 0.01, p = 0.02, p = 0.01, p = 0.009, p = 0.002, p = 0.02, respectively). There was a statistically significant negative correlation between best-corrected visual acuity (BCVA) and AI (p = 0.02), and a statistically significant positive correlation between peripapillary vascular density and BCVA (p = 0.04). Conclusions: We consider that the lower retinal, choriocapillaris, ODVD values, and retinal and RNFL thicknesses in the patients with IMT compared to the controls were due to vascular damage, remodeling, fibrosis, proliferation, and Müller cell damage. Ellipsoid zone defect, AI, and peripapillary vascular density are important indicators in the evaluation of visual acuity in these patients.

16

Parrozzani, Raffaele, Francesca Leonardi, Luisa Frizziero, Eva Trevisson, Maurizio Clementi, Elisabetta Pilotto, Stefano Fusetti, Giacomo Miglionico, and Edoardo Midena. "Retinal Vascular and Neural Remodeling Secondary to Optic Nerve Axonal Degeneration." Ophthalmology Retina 2, no. 8 (August 2018): 827–35. http://dx.doi.org/10.1016/j.oret.2017.12.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Jung, S., D. Kannenkeril, C. Ott, R. Cífková, J. M. Harazny, and R. E. Schmieder. "VASCULAR REMODELING OF RETINAL VESSELS IN PATIENTS WITH CONGESTIVE HEART FAILURE." Journal of Hypertension 37 (July 2019): e212. http://dx.doi.org/10.1097/01.hjh.0000572728.34473.c3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Behar-Cohen, F., D. BenEzra, G. Soubrane, L. Jonet, and J. C. Jeanny. "Krypton laser photocoagulation induces retinal vascular remodeling rather than choroidal neovascularization." Experimental Eye Research 83, no. 2 (August 2006): 263–75. http://dx.doi.org/10.1016/j.exer.2005.12.010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Ott*, Christian, Agnes Jumar, Joanna Harazny, Stephanie Schmidt, and Roland Schmieder. "4.1 EFFECT OF ALISKIREN ON VASCULAR REMODELING IN SMALL RETINAL CIRCULATION." Artery Research 12, no. C (2015): 44. http://dx.doi.org/10.1016/j.artres.2015.10.020.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Luisi, Jonathan, Wei Liu, Wenbo Zhang, and Massoud Motamedi. "En-Face Optical Coherence Tomography Angiography for Longitudinal Monitoring of Retinal Injury." Applied Sciences 9, no. 13 (June 28, 2019): 2617. http://dx.doi.org/10.3390/app9132617.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

A customized Optical Coherence Tomography Angiography (OCTA) algorithm and Orthogonal OCT (en-face and B-Scans) were used for longitudinal assessment of retina murine vascular and tissue remodeling comparing photoreceptor ablation and laser-induced Choroidal Neovascularization (CNV). In the mouse model, we utilized a combined OCTA/OCT technique to image and quantify morphological and vascular features of laser lesions over time. This approach enabled us to monitor and correlate the dynamics of retina vascular and tissue remodeling as evidenced by swelling, edema, and scarring. From the OCT B-Scans, three stages of inflammatory progression were identified: the early response occurring within hours to day 3, the transition phase from 3–7 days, and the late stage of 7–21 days entering either the resolving phase or chronic phase, respectively. For the case of CNV, en-face OCTA revealed a transient non-perfusion of inner retina capillaries, specifically Deep Vascular Plexus (DVP), which corresponded to growth in lesions of a height of 200 µm or greater. Non-perfusion first occurred at 24 hours, persisted during edema and CNV formation days 7–14. In contrast, the acute inflammation induced photoreceptor damage, but no detectable alterations to the microvasculature were observed. We demonstrated that the en-face OCTA system is capable of visualizing capillary networks (∼5 µm) and the corresponding tissue remodeling and growth dynamics allowing for separating acute injury from CNV. For the first time, by using OCTA we observed the presence of the 5–10 μm capillary non-perfusion present in DVP as part of CNV formation and the associated wound healing in the retina.

21

Temkar, Shreyas, Geeta Behera, Hemanth Ramachandar, Disha Agarwal, Mary Stephen, and Amit Kumar Deb. "Expeditious resolution of disc and iris neovascularization." Indian Journal of Ophthalmology - Case Reports 4, no. 2 (April 2024): 425–27. http://dx.doi.org/10.4103/ijo.ijo_3203_23.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Intraocular neovascularization is seen commonly as a response to retinal ischemia or less commonly due to inflammation. Inflammatory iris neovascularization responds well to topical steroids, whereas retinal neovascularization associated with uveitic conditions responds to systemic steroids or periocular depot injections. This case highlights an unusually rapid resolution of disc neovascularization along with iris neovascularization just with topical steroids in a middle-aged lady diagnosed with bilateral panuveitis and retinal vasculitis. We presume it may be due to a spontaneous decrease in posterior segment inflammation or due to systemic vascular remodeling.

22

Roy, S., K. Trudeau, S. Roy, Y. Behl, S. Dhar, and A. Chronopoulos. "New Insights into Hyperglycemia-induced Molecular Changes in Microvascular Cells." Journal of Dental Research 89, no. 2 (December 30, 2009): 116–27. http://dx.doi.org/10.1177/0022034509355765.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Hyperglycemia is the most prevalent characteristic of diabetes and plays a central role in mediating adverse effects on vascular cells during the progression of diabetic vascular complications. In diabetic microangiopathy, hyperglycemia induces biochemical and molecular changes in microvascular cells that ultimately progress to retinal, renal, and neural complications and extends to other complications, including advanced periodontal disease. In this review, we describe changes involving basement membrane thickening, tissue remodeling, gap junctions, inflammation, cytokines, and transcription factors, and their effects on the pathogenesis of diabetic microvascular complications. The majority of the changes described relate to retinal microangiopathy, since ultrastructural, structural, and biochemical alterations have been well-characterized in this tissue.

23

Sadowski, Janusz, Ryszard Targonski, Piotr Cyganski, Paulina Nowek, Magdalena Starek-Stelmaszczyk, Katarzyna Zajac, Judyta Juranek, Joanna Wojtkiewicz, and Andrzej Rynkiewicz. "Remodeling of Retinal Arterioles and Carotid Arteries in Heart Failure Development—A Preliminary Study." Journal of Clinical Medicine 11, no. 13 (June 27, 2022): 3721. http://dx.doi.org/10.3390/jcm11133721.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Current data indicate that heart failure (HF) is associated with inflammation and microvascular dysfunction and remodeling. These mechanisms could be involved in HF development and progression, especially in HF with preserved ejection fraction (HFpEF). We aimed to compare structural changes in retinal arterioles and carotid arteries between HF patients and patients without heart failure. This preliminary, retrospective, case-control study included 28 participants (14 patients with HFpEF and 14 age- and sex-matched healthy controls). Carotid intima-media thickness to lumen ratio (cIMTLR) was assessed using B-mode ultrasonography. Retinal arterioles wall- to-lumen ratio (rWLR) was assessed by adaptive optics camera rtx1. The HF patients had higher IMTLR (Δmedian [HFpEF–control group] 0.07, p = 0.01) and eWLR (Δmedian 0.03, p = 0.001) in comparison to patients without HF. In the whole study group, rWLR correlated significantly with IMTLR (r = 0.739, p = 0.001). Prevalence of arterial hypertension was similar in both groups, however, patients with HF had a significantly lower office, central and 24-h ambulatory blood pressure (systolic Δmedian −21 to −18 mmHg; diastolic Δmedian −23 to −10 mmHg). Our data suggests gradual and simultaneous progression of vascular remodeling in both retinal arterioles and carotid arteries in HFpEF patients. This process could be a marker of HF development. Significantly lower blood pressure values in HF group may indicate that vascular remodeling could be independent of BP control. Nevertheless, further and larger prospective studies allowing to reduce the impact of confounding and address temporality are warranted.

24

Ho, Sze Yuan, Yuet Ping Kwan, Beiying Qiu, Alison Tan, Hannah Louise Murray, Veluchamy Amutha Barathi, Nguan Soon Tan, et al. "Investigating the Role of PPARβ/δ in Retinal Vascular Remodeling Using Pparβ/δ-Deficient Mice." International Journal of Molecular Sciences 21, no. 12 (June 20, 2020): 4403. http://dx.doi.org/10.3390/ijms21124403.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Peroxisome proliferator-activated receptor (PPAR)β/δ is a member of the nuclear receptor superfamily of transcription factors, which plays fundamental roles in cell proliferation and differentiation, inflammation, adipogenesis, and energy homeostasis. Previous studies demonstrated a reduced choroidal neovascularization (CNV) in Pparβ/δ-deficient mice. However, PPARβ/δ’s role in physiological blood vessel formation and vessel remodeling in the retina has yet to be established. Our study showed that PPARβ/δ is specifically required for disordered blood vessel formation in the retina. We further demonstrated an increased arteriovenous crossover and wider venous caliber in Pparβ/δ-haplodeficient mice. In summary, these results indicated a critical role of PPARβ/δ in pathological angiogenesis and blood vessel remodeling in the retina.

25

Qian, Xiu Qing, Kun Ya Zhang, Zi Hang Liu, and Zhi Cheng Liu. "Three Remodeling of the Optical Nerve Head Including Retinal Blood Vessel Based on Live Animal Experiment." Applied Mechanics and Materials 275-277 (January 2013): 2673–76. http://dx.doi.org/10.4028/www.scientific.net/amm.275-277.2673.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

With increasing evidence that vascular risk factors play a role in the development of glaucoma, it is critical to be familiar with factors related to intraocular blood flow. It is important to obtain that the modal of the optical never head including the retinal blood vessel. The images optical never head of a cat using the optical coherence tomography images were obtained. Then, the three modal of the optical never head and the retinal blood vessel were reconstructed using the technology of image process, respectively. The three-dimensional modal of optical nerve head including retinal blood vessel could get using Boolean Operation.

26

Sinha, Debasish, Andrew Klise, Yuri Sergeev, Stacey Hose, Imran A. Bhutto, Laszlo Hackler, Tanya Malpic-llanos, et al. "βA3/A1-crystallin in astroglial cells regulates retinal vascular remodeling during development." Molecular and Cellular Neuroscience 37, no. 1 (January 2008): 85–95. http://dx.doi.org/10.1016/j.mcn.2007.08.016.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Ishida, Susumu, Kenji Yamashiro, Tomohiko Usui, Yuichi Kaji, Yuichiro Ogura, Tetsuo Hida, Yoshihito Honda, Yoshihisa Oguchi, and Anthony P. Adamis. "Leukocytes mediate retinal vascular remodeling during development and vaso-obliteration in disease." Nature Medicine 9, no. 6 (May 5, 2003): 781–88. http://dx.doi.org/10.1038/nm877.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Katsi, V., G. Souretis, C. Vlachopoulos, N. Alexopoulos, K. Benekos, I. Vlasseros, D. Tousoulis, C. Stefanadis, and I. Kallikazaros. "RETINAL VASCULAR DETERIORATION IS ACCOMPANIED BY ADVERSE CARDIAC REMODELING IN ESSENTIAL HYPERTENSION." Journal of Hypertension 29 (June 2011): e503. http://dx.doi.org/10.1097/00004872-201106001-01527.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Cohen, Steven M. "Vascular Remodeling in Central Retinal Vein Occlusion Following Laser-Induced Chorioretinal Anastomosis." JAMA Ophthalmology 131, no. 3 (March 1, 2013): 403. http://dx.doi.org/10.1001/2013.jamaophthalmol.530.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Binet, François, Gael Cagnone, Sergio Crespo-Garcia, Masayuki Hata, Mathieu Neault, Agnieszka Dejda, Ariel M. Wilson, et al. "Neutrophil extracellular traps target senescent vasculature for tissue remodeling in retinopathy." Science 369, no. 6506 (August 20, 2020): eaay5356. http://dx.doi.org/10.1126/science.aay5356.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

In developed countries, the leading causes of blindness such as diabetic retinopathy are characterized by disorganized vasculature that can become fibrotic. Although many such pathological vessels often naturally regress and spare sight-threatening complications, the underlying mechanisms remain unknown. Here, we used orthogonal approaches in human patients with proliferative diabetic retinopathy and a mouse model of ischemic retinopathies to identify an unconventional role for neutrophils in vascular remodeling during late-stage sterile inflammation. Senescent vasculature released a secretome that attracted neutrophils and triggered the production of neutrophil extracellular traps (NETs). NETs ultimately cleared diseased endothelial cells and remodeled unhealthy vessels. Genetic or pharmacological inhibition of NETosis prevented the regression of senescent vessels and prolonged disease. Thus, clearance of senescent retinal blood vessels leads to reparative vascular remodeling.

31

Lemoli, Matteo, Claudia Agabiti Rosei, Claudia Rossini, Andrea Delbarba, Nicola Laera, Paolo Facondo, Matteo Nardin, et al. "RETINAL MICROVASCULAR ALTERATIONS IN PATIENTS WITH ERECTILE DYSFUNCTION." Journal of Hypertension 42, Suppl 1 (May 2024): e304. http://dx.doi.org/10.1097/01.hjh.0001022664.67310.94.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Objective: The presence of erectile dysfunction (ED) is related with the subsequent occurrence of cardiovascular (CV) disease, in ED forms with a predominantly vascular component. The presence of penile arterial damage, assessed by dynamic penile echo color doppler, doubles the risk of a subsequent CV event. Microvascular alterations, and in particular the increase in the tunica-media-to-lumen ratio (M/L) of subcutaneous small arteries or in the wall-to-lumen ratio (WLR) of retinal arterioles, are present in several clinical conditions, including hypertension, and are predictors of CV events. The aim of this study is to evaluate the possible presence of structural alterations of the retinal microcirculation in patients with vascular ED assessed through dynamic penile echo color doppler. Design and method: Patients attending the Endocrinology outpatient clinics of the ASST Spedali Civili in Brescia undergoing dynamic penile echo color doppler to determine the vascular or non-vascular etiology of ED were included in the study. The patients underwent an evaluation of the capillary density at the dorsum of the fourth finger, by capillaroscopy, and an evaluation of the retinal microcirculation through Adaptive Optics to assess the WLR and the wall cross-sectional area (WCSA) of the retinal arterioles. Results: A total of 33 patients were included in the study: 10 patients (30.3%) had vascular ED and 23 (69.7%) had non vascular ED. The characteristics of the patients are shown in the Table. A higher prevalence of the main cardiovascular risk factors was observed in patients with vascular ED, although none of them reached statistical significance. No difference in basal or total (after venous congestion) capillary density was observed. Evaluation of the retinal arteriole morphology showed a significantly increased WLR in patients with vascular-based ED compared to patients with non vascular ED (0.29 vs. 0.26, p=0.031) with no difference in WCSA, thus indicating eutrophic remodeling. Conclusions: Our preliminary data highlight a potential correlation between arterial vascular changes present in the penile circulation and retinal microcirculation, suggesting the possibility of common damage mechanisms and new potential elements of population risk stratification.

32

Aissopou, Evaggelia K., Vasiliki-Kalliopi Bournia, Athanase D. Protogerou, Stylianos Panopoulos, Theodoros G. Papaioannou, Panayiotis G. Vlachoyiannopoulos, Marco Matucci-Cerinic, and Petros P. Sfikakis. "Intact Calibers of Retinal Vessels in Patients with Systemic Sclerosis." Journal of Rheumatology 42, no. 4 (February 1, 2015): 608–13. http://dx.doi.org/10.3899/jrheum.141425.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Objective.A primary endothelial cell dysfunction is thought to be involved in systemic sclerosis (SSc)-associated fibroproliferative vasculopathy of the microcirculation and small arterioles, even in sites not affected by fibrosis. Because the role of fibroblasts in pathologic modifications and vascular wall remodeling is relatively unclear, and because the retina provides a unique opportunity to assess microcirculation in the absence of resident fibroblasts, we systematically evaluated retinal vessels in patients with SSc.Methods.Digital retinal images were obtained from both eyes of 93 consecutive patients with fully characterized SSc and 29 healthy controls matched 1:1 for age and sex with selected patients without diabetes, hypertension history, or antihypertensive treatment. Internal microvascular calibers (erythrocyte column width in μm) by central retinal arteriolar and venular equivalents and arteriolar to venular ratio were measured using validated software.Results.Arteriolar and venular calibers were similar in patients and their matched controls (mean ± SEM; 187 ± 2 vs 184 ± 3, p = 0.444, and 211 ± 2 vs 216 ± 3, p = 0.314, respectively). Both arteriolar and venular calibers and their ratio in patients with SSc were not associated with disease duration, extent of skin involvement, pulmonary fibrosis, digital ulcers or pitting scars, amputations, digital capillaroscopic findings, inflammatory indices, or autoantibodies.Conclusion.The evidence that retinal microcirculation is spared in SSc suggests that fibroproliferative vasculopathy may depend on specific cellular or soluble factors not present in the retinal environment.

33

Liu, Chang, Hui-Min Ge, Bai-Hui Liu, Rui Dong, Kun Shan, Xue Chen, Mu-Di Yao, et al. "Targeting pericyte–endothelial cell crosstalk by circular RNA-cPWWP2A inhibition aggravates diabetes-induced microvascular dysfunction." Proceedings of the National Academy of Sciences 116, no. 15 (March 26, 2019): 7455–64. http://dx.doi.org/10.1073/pnas.1814874116.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

The crosstalk between vascular pericytes and endothelial cells (ECs) is critical for microvascular stabilization and remodeling; however, the crosstalk is often disrupted by diabetes, leading to severe and even lethal vascular damage. Circular RNAs are a class of endogenous RNAs that regulate several important physiological and pathological processes. Here we show that diabetes-related stress up-regulates cPWWP2A expression in pericytes but not in ECs. In vitro studies show that cPWWP2A directly regulates pericyte biology but indirectly regulates EC biology via exosomes carrying cPWWP2A. cPWWP2A acts as an endogenous miR-579 sponge to sequester and inhibit miR-579 activity, leading to increased expression of angiopoietin 1, occludin, and SIRT1. In vivo studies show that cPWWP2A overexpression or miR-579 inhibition alleviates diabetes mellitus-induced retinal vascular dysfunction. By contrast, inhibition of cPWWP2A-mediated signaling by silencing cPWWP2A or overexpressing miR-579 aggravates retinal vascular dysfunction. Collectively, this study unveils a mechanism by which pericytes and ECs communicate. Intervention of cPWWP2A or miR-579 expression may offer opportunities for treating diabetic microvascular complications.

34

Ohnuki, Hidetaka, Hirofumi Inoue, Nobuaki Takemori, Hironao Nakayama, Tomohisa Sakaue, Shinji Fukuda, Daisuke Miwa, et al. "BAZF, a novel component of cullin3-based E3 ligase complex, mediates VEGFR and Notch cross-signaling in angiogenesis." Blood 119, no. 11 (March 15, 2012): 2688–98. http://dx.doi.org/10.1182/blood-2011-03-345306.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Abstract Angiogenic homeostasis is maintained by a balance between vascular endothelial growth factor (VEGF) and Notch signaling in endothelial cells (ECs). We screened for molecules that might mediate the coupling of VEGF signal transduction with down-regulation of Notch signaling, and identified B-cell chronic lymphocytic leukemia/lymphoma6-associated zinc finger protein (BAZF). BAZF was induced by VEGF-A in ECs to bind to the Notch signaling factor C-promoter binding factor 1 (CBF1), and to promote the degradation of CBF1 through polyubiquitination in a CBF1-cullin3 (CUL3) E3 ligase complex. BAZF disruption in vivo decreased endothelial tip cell number and filopodia protrusion, and markedly abrogated vascular plexus formation in the mouse retina, overlapping the retinal phenotype seen in response to Notch activation. Further, impaired angiogenesis and capillary remodeling were observed in skin-wounded BAZF−/− mice. We therefore propose that BAZF supports angiogenic sprouting via BAZF-CUL3-based polyubiquitination-dependent degradation of CBF1 to down-regulate Notch signaling.

35

Kouroupaki, A. I., E. Pateras, and K. Karabatsas. "Quantitative Measurements of Macular and Optic Nerve Head Blood Flow Parameters Following Cataract Surgery in Eye Department, Red Cross Tertiary General Hospital, Athens, Greece." Ophthalmology Research: An International Journal 18, no. 2 (April 22, 2023): 30–37. http://dx.doi.org/10.9734/or/2023/v18i2383.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Objective: To evaluate the effect of uncomplicated cataract surgery on macular and optic nerve head blood flow with Optical Coherence Tomography Angiography (OCT-A). Retinal vascular changes and macular vessel remodeling following cataract surgery is an area of interest, as the effect, cause and duration of such changes remain debatable. Setting: Eye Department, Red Cross Tertiary General Hospital, Athens, Greece. Methods: In this study, we recruited cataract surgery candidates who had regular post operative visits and underwent longitudinal OCT-A examinations before and after surgery. Results: Macular vessel density increased in the post operative visits both in the superficial (SCP) and deep capillary network (DCP) (P<0.001) and showed a persistent effect over 3 months follow-up. Macular thickness increased over the first postoperative month, but returned to preoperative values at 3 months. Foveal avascular zone (FAZ) measurements and vessel density at radial peripapillary capillaries (RPC) were unaffected. Conclusions: OCT-A enables a quantitative analysis of blood flow by regular patient monitoring. In this study, we found that after cataract surgery, macular blood flow increased significantly. The reason for this could be attributed to post operative inflammatory process or vascular remodeling due to change in retinal metabolic demands.

36

Diem, Clemens, Cengiz Türksever, and Margarita G. Todorova. "The Presence of Hyperreflective Foci Reflects Vascular, Morphologic and Metabolic Alterations in Retinitis Pigmentosa." Genes 13, no. 11 (November 4, 2022): 2034. http://dx.doi.org/10.3390/genes13112034.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Background: The presence of hyperreflective foci (HRF) in retinitis pigmentosa (RP) is a potentially new finding. We investigated the presence of HRF in SD-OCT images in eyes with RP and its relation to vascular, morphologic and metabolic findings in RP. Methods: The study was performed on 42 RP patients and 24 controls. Using SD-OCT, we calculated the amount of HRF within the entire retina (HRF-ER) and the outer nuclear layer (HRF-ONL). Retinal vessel diameters (μm) and oxygen saturation (%) values were measured using Oxymap T1. We evaluated the mean diameter in retinal arterioles (D-A) and venules (D-V), the corresponding oxygen saturation values (A-SO2, V-SO2) and the oxygen saturation difference (A-V SO2). Results: RP differed from controls by HRF-ER, HRF-ON and EZ-length (p < 0.001). D-A and D-V were narrower and A-SO2 and V-SO2 were higher in RP (p ≤ 0.001). Within RP, significant interactions were found between the HRF-ER* group and: BCVA, EZ length, D-A, A-SO2 and A-V SO2 (p ≤ 0.018). The HRF-ONL* group interactions were significant for: BCVA, EZ length, D-A, A-SO2 and A-V SO2 (p ≤ 0.014). Conclusion: The present study highlights the presence of HRF to reflect the vascular, morphologic and metabolic alterations in RP. These biomarkers seem to be associated with remodeling and apoptosis that occur with the progression of degeneration.

37

Mazzoni, Jenna, Julian R. Smith, Sanjid Shahriar, Tyler Cutforth, Bernardo Ceja, and Dritan Agalliu. "The Wnt Inhibitor Apcdd1 Coordinates Vascular Remodeling and Barrier Maturation of Retinal Blood Vessels." Neuron 96, no. 5 (December 2017): 1055–69. http://dx.doi.org/10.1016/j.neuron.2017.10.025.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Ott, Christian, Ulrike Raff, Joanna M. Harazny, Georg Michelson, and Roland E. Schmieder. "Central Pulse Pressure Is an Independent Determinant of Vascular Remodeling in the Retinal Circulation." Hypertension 61, no. 6 (June 2013): 1340–45. http://dx.doi.org/10.1161/hypertensionaha.111.00617.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Gehlbach, P., S. Hose, B. Lei, C. Zhang, M. Cano, M. Arora, R. Neal, et al. "Developmental abnormalities in the Nuc1 rat retina: A spontaneous mutation that affects neuronal and vascular remodeling and retinal function." Neuroscience 137, no. 2 (January 2006): 447–61. http://dx.doi.org/10.1016/j.neuroscience.2005.08.084.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Chrzanowska-Wodnicka, Magdalena, Anna E. Kraus, Daniel Gale, Gilbert C. White, and Jillian VanSluys. "Defective angiogenesis, endothelial migration, proliferation, and MAPK signaling in Rap1b-deficient mice." Blood 111, no. 5 (March 1, 2008): 2647–56. http://dx.doi.org/10.1182/blood-2007-08-109710.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Angiogenesis is the main mechanism of vascular remodeling during late development and, after birth, in wound healing. Perturbations of angiogenesis occur in cancer, diabetes, ischemia, and inflammation. While much progress has been made in identifying factors that control angiogenesis, the understanding of the precise molecular mechanisms involved is incomplete. Here we identify a small GTPase, Rap1b, as a positive regulator of angiogenesis. Rap1b-deficient mice had a decreased level of Matrigel plug and neonatal retinal neovascularization, and aortas isolated from Rap1b-deficient animals had a reduced microvessel sprouting response to 2 major physiological regulators of angiogenesis: vascular endothelial growth factor (VEGF) and basic fibroblasts growth factor (bFGF), indicating an intrinsic defect in endothelial cells. Proliferation of retinal endothelial cells in situ and in vitro migration of lung endothelial cells isolated from Rap1b-deficient mice were inhibited. At the molecular level, activation of 2 MAP kinases, p38 MAPK and p42/44 ERK, important regulators of endothelial migration and proliferation, was decreased in Rap1b-deficient endothelial cells in response to VEGF stimulation. These studies provide evidence that Rap1b is required for normal angiogenesis and reveal a novel role of Rap1 in regulation of proangiogenic signaling in endothelial cells.

41

Katsi, V., G. Souretis, I. Skiadas, C. Vlachopoulos, D. Tsartsalis, D. Tousoulis, C. Stefanadis, and I. Kallikazaros. "RETINAL VASCULAR DAMAGE AND CARDIAC REMODELING IN ESSENTIAL HYPERTENSION: A TALE OF PARALLEL ESCALATION: PP.35.445." Journal of Hypertension 28 (June 2010): e583. http://dx.doi.org/10.1097/01.hjh.0000379983.44380.18.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Bottoni, Ferdinando, Mary Romano, Amedeo Massacesi, and Fulvio Bergamini. "Remodeling of the vascular channels in retinal angiomatous proliferations treated with intravitreal triamcinolone acetonide and photodynamic therapy." Graefe's Archive for Clinical and Experimental Ophthalmology 244, no. 11 (April 12, 2006): 1528–33. http://dx.doi.org/10.1007/s00417-006-0311-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Takase, Haruka, Ken Matsumoto, Rie Yamadera, Yoshiaki Kubota, Ayaka Otsu, Rumiko Suzuki, Hiroyuki Ishitobi, et al. "Genome-wide identification of endothelial cell–enriched genes in the mouse embryo." Blood 120, no. 4 (July 26, 2012): 914–23. http://dx.doi.org/10.1182/blood-2011-12-398156.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Abstract The early blood vessels of the embryo and yolk sac in mammals develop by aggregation of de novo–forming angioblasts into a primitive vascular plexus, which then undergoes a complex remodeling process. Angiogenesis is also important for disease progression in the adult. However, the precise molecular mechanism of vascular development remains unclear. It is therefore of great interest to determine which genes are specifically expressed in developing endothelial cells (ECs). Here, we used Flk1-deficient mouse embryos, which lack ECs, to perform a genome-wide survey for genes related to vascular development. We identified 184 genes that are highly enriched in developing ECs. The human orthologs of most of these genes were also expressed in HUVECs, and small interfering RNA knockdown experiments on 22 human orthologs showed that 6 of these genes play a role in tube formation by HUVECs. In addition, we created Arhgef15 knockout and RhoJ knockout mice by a gene-targeting method and found that Arhgef15 and RhoJ were important for neonatal retinal vascularization. Thus, the genes identified in our survey show high expression in ECs; further analysis of these genes should facilitate our understanding of the molecular mechanisms of vascular development in the mouse.

44

Somfai, Gabor, Thalmon Campagnoli, Jing Tian, Heinrich Gerding, William Smiddy, and Delia DeBuc. "The Assessment of Blood Flow Velocities in Retinal Collaterals in Diabetic Retinopathy." Klinische Monatsblätter für Augenheilkunde 236, no. 04 (April 2019): 530–35. http://dx.doi.org/10.1055/a-0861-9675.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Abstract Purpose Diabetic retinopathy (DR) is a microvascular disease characterized by capillary dropout and resultant retinal ischemia which then leads to retinal vascular remodeling. Our goal was to assess blood flow velocities in retinal collateral vessels in healthy and diabetic subjects with various stages of DR. Methods In our pilot study, we enrolled five eyes of five healthy subjects (H), five eyes of four subjects with diabetes and no retinopathy (DM), three eyes of three subjects with mild non-proliferative diabetic retinopathy (MDR), and five eyes of four subjects with proliferative diabetic retinopathy (PDR). Following routine ophthalmic examination, all subjects were imaged using a retinal function imager (RFI; Optical Imaging Inc., Rehovot, Israel). The built-in software of the RFI was used to identify and segment retinal collaterals with measurement of the blood flow velocities (BFV). One-way ANOVA was performed for BFV, followed by Newman-Keuls post hoc test. The level of significance was set at 5%. Results The total number of collateral segments involved in the study was 30, 31, 21, and 39 in the H, DM, MDR, and PDR groups, respectively. The BFVs in the collaterals were significantly lower in PDR (H: 1.86 ± 0.67, DM: 1.91 ± 0.71, MDR: 1.71 ± 0.53, PDR: 1.37 ± 0.58 mm/s). The PDR group showed a statistically significant difference in the comparisons to all groups (p = 0.012, p = 0.008, and p = 0.043 for the H, DM, and MDR groups, respectively), while no other comparisons between the groups were significant. Conclusion We observed decreased BFV in retinal collaterals in PDR that may be due to the extensive capillary dropout and retinal ischemia. Further studies are needed for the noninvasive functional assessment of retinal microvascular changes in DR to better understand the underlying pathophysiology.

45

MITAMURA, MIZUHO, SATORU KASE, and SUSUMU ISHIDA. "Multimodal Imaging, Including Laser Speckle Flowgraphy: A Case of Retinal Metastasis." Cancer Diagnosis & Prognosis 4, no. 4 (July 1, 2024): 539–43. http://dx.doi.org/10.21873/cdp.10361.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Background/Aim: Intraocular metastases of systemic cancer are most frequently located in the choroid, followed by the iris and ciliary body, while retinal metastases are extremely rare. Here we present a case of retinal metastasis and analyze multimodal imaging. Case Report: A 66-year-old woman with a medical history of breast cancer 5 years earlier was referred to our Department struggling with blurry vision in her right eye. At initial examination, her best-corrected visual acuity (BCVA) was 1.0 oculus dexter (OD). Fundus examination revealed a yellowish elevated lesion with irregular surface, measuring 2 papillary diameters, along with serous retinal detachment (SRD) on the temporal side of the optic disc. Optical coherence tomography showed SRD with an isointense nodule extending across all retinal layers. Fluorescein angiography showed hyperfluorescence and vigorous fluorescence leakage inside the tumor in the early and late phases, respectively. Indocyanine green angiography depicted feeder and drainage vessels within the mass. Laser speckle flowgraphy (LSFG) showed a cold signal inside the tumor. Based on these clinical findings, the mass was diagnosed as a retinal metastasis. Eight days after the initial visit, the patient underwent external beam radiation to the right eye. One month after the initial diagnosis, her BCVA was 0.7 OD, the tumor was localized, and SRD had decreased. LSFG indicated vascular remodeling with marginally warmer signals in the tumor. Conclusion: LSFG of the retinal metastasis showed a cold signal, suggesting low tumor blood flow velocity and that the tumor may have grown slowly. LSFG findings are likely to play a supportive role in clinical diagnosis and contribute to better understanding of pathogenesis in juxtapapillary tumors.

46

Tripathy, Swetapadma, Hong-Gam Le, Maria Vittoria Cicinelli, and Manjot K. Gill. "Longitudinal Changes on Optical Coherence Tomography Angiography in Retinal Vein Occlusion." Journal of Clinical Medicine 10, no. 7 (April 1, 2021): 1423. http://dx.doi.org/10.3390/jcm10071423.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Background: To evaluate the longitudinal changes on optical coherence tomography angiography (OCTA) in retinal vein occlusion (RVO). Methods: Retrospective study of patients with RVO treated with intravitreal anti-vascular endothelial growth factors (VEGF) for macular edema. Foveal avascular zone (FAZ) area, vessel density (VD), vessel length density (VLD), and adjusted flow index (AFI) were calculated. The unaffected eye of each participant was used as a control. Results: Twelve RVO eyes were included, receiving 6 ± 3 anti-VEGF injections over a follow-up of 10.4 ± 3.1 months. Compared to fellow eyes, RVO eyes had lower VD and VLD at inclusion (p = 0.07 and p = 0.04) and last visit (p = 0.002 and p < 0.001). VD, AFI, and VLD did not change over time, while FAZ area increased in RVO eyes (+0.016 ± 0.024 mm2, p = 0.04). AFI correlated with duration of disease (r = 0.63, p = 0.02). Visual acuity was inversely related to VD and VLD over the follow-up. Conclusions: OCTA parameters remained stable with sustained anti-VEGF treatment in RVO, while changes in the FAZ area may suggest capillary remodeling after RVO.

47

Segarra, Marta, Hidetaka Ohnuki, Dragan Maric, Ombretta Salvucci, Xu Hou, Anil Kumar, Xuri Li, and Giovanna Tosato. "Semaphorin 6A regulates angiogenesis by modulating VEGF signaling." Blood 120, no. 19 (November 8, 2012): 4104–15. http://dx.doi.org/10.1182/blood-2012-02-410076.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Abstract Formation of new vessels during development and in the mature mammal generally proceeds through angiogenesis. Although a variety of molecules and signaling pathways are known to underlie endothelial cell sprouting and remodeling during angiogenesis, many aspects of this complex process remain unexplained. Here we show that the transmembrane semaphorin6A (Sema6A) is expressed in endothelial cells, and regulates endothelial cell survival and growth by modulating the expression and signaling of VEGFR2, which is known to maintain endothelial cell viability by autocrine VEGFR signaling. The silencing of Sema6A in primary endothelial cells promotes cell death that is not rescued by exogenous VEGF-A or FGF2, attributable to the loss of prosurvival signaling from endogenous VEGF. Analyses of mouse tissues demonstrate that Sema6A is expressed in angiogenic and remodeling vessels. Mice with null mutations of Sema6A exhibit significant defects in hyaloid vessels complexity associated with increased endothelial cell death, and in retinal vessels development that is abnormally reduced. Adult Sema6A-null mice exhibit reduced tumor, matrigel, and choroidal angiogenesis compared with controls. Sema6A plays important roles in development of the nervous system. Here we show that it also regulates vascular development and adult angiogenesis.

48

Rizzoni, Damiano, Claudia Agabiti-Rosei, Gianluca E. M. Boari, Maria Lorenza Muiesan, and Carolina De Ciuceis. "Microcirculation in Hypertension: A Therapeutic Target to Prevent Cardiovascular Disease?" Journal of Clinical Medicine 12, no. 15 (July 25, 2023): 4892. http://dx.doi.org/10.3390/jcm12154892.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Arterial hypertension is a common condition worldwide and an important risk factor for cardio- and cerebrovascular events, renal diseases, as well as microvascular eye diseases. Established hypertension leads to the chronic vasoconstriction of small arteries as well as to a decreased lumen diameter and the thickening of the arterial media or wall with a consequent increased media-to-lumen ratio (MLR) or wall-to-lumen ratio (WLR). This process, defined as vascular remodeling, was firstly demonstrated in small resistance arteries isolated from subcutaneous biopsies and measured by micromyography, and this is still considered the gold-standard method for the assessment of structural alterations in small resistance arteries; however, microvascular remodeling seems to represent a generalized phenomenon. An increased MLR may impair the organ flow reserve, playing a crucial role in the maintenance and, probably, also in the progressive worsening of hypertensive disease, as well as in the development of hypertension-mediated organ damage and related cardiovascular events, thus possessing a relevant prognostic relevance. New non-invasive techniques, such as scanning laser Doppler flowmetry or adaptive optics, are presently under development, focusing mainly on the evaluation of WLR in retinal arterioles; recently, also retinal microvascular WLR was demonstrated to have a prognostic impact in terms of cardio- and cerebrovascular events. A rarefaction of the capillary network has also been reported in hypertension, which may contribute to flow reduction in and impairment of oxygen delivery to different tissues. These microvascular alterations seem to represent an early step in hypertension-mediated organ damage since they might contribute to microvascular angina, stroke, and renal dysfunction. In addition, they can be markers useful in monitoring the beneficial effects of antihypertensive treatment. Additionally, conductance arteries may be affected by a remodeling process in hypertension, and an interrelationship is present in the structural changes in small and large conductance arteries. The review addresses the possible relations between structural microvascular alterations and hypertension-mediated organ damage, and their potential improvement with antihypertensive treatment.

49

Kim, E. Seul, Min Sang Lee, Hayoung Jeong, Su Yeon Lim, Doha Kim, Dahwun Kim, Jaeback Jung, et al. "Sustained-Release Microspheres of Rivoceranib for the Treatment of Subfoveal Choroidal Neovascularization." Pharmaceutics 13, no. 10 (September 24, 2021): 1548. http://dx.doi.org/10.3390/pharmaceutics13101548.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

The wet type of age-related macular degeneration (AMD) accompanies the subfoveal choroidal neovascularization (CNV) caused by the abnormal extension or remodeling of blood vessels to the macula and retinal pigment epithelium (RPE). Vascular endothelial growth factor (VEGF) is known to play a crucial role in the pathogenesis of the disease. In this study, we tried to repurpose an investigational anticancer drug, rivoceranib, which is a selective inhibitor of VEGF receptor-2 (VEGFR2), and evaluate the therapeutic potential of the drug for the treatment of wet-type AMD in a laser-induced CNV mouse model using microsphere-based sustained drug release formulations. The PLGA-based rivoceranib microsphere can carry out a sustained delivery of rivoceranib for 50 days. When administered intravitreally, the sustained microsphere formulation of rivoceranib effectively inhibited the formation of subfoveal neovascular lesions in mice.

50

Mahmoud, Marwa, Ian M. Evans, Vedanta Mehta, Caroline Pellet-Many, Ketevan Paliashvili, and Ian Zachary. "Smooth muscle cell-specific knockout of neuropilin-1 impairs postnatal lung development and pathological vascular smooth muscle cell accumulation." American Journal of Physiology-Cell Physiology 316, no. 3 (March 1, 2019): C424—C433. http://dx.doi.org/10.1152/ajpcell.00405.2018.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Abstract:

Neuropilin 1 (NRP1) is important for neuronal and cardiovascular development due to its role in conveying class 3 semaphorin and vascular endothelial growth factor signaling, respectively. NRP1 is expressed in smooth muscle cells (SMCs) and mediates their migration and proliferation in cell culture and is implicated in pathological SMC remodeling in vivo. To address the importance of Nrp1 for SMC function during development, we generated conditional inducible Nrp1 SMC-specific knockout mice. Induction of early postnatal SMC-specific Nrp1 knockout led to pulmonary hemorrhage associated with defects in alveogenesis and revealed a specific requirement for Nrp1 in myofibroblast recruitment to the alveolar septae and PDGF-AA-induced migration in vitro. Furthermore, SMC-specific Nrp1 knockout inhibited PDGF-BB-stimulated SMC outgrowth ex vivo in aortic ring assays and reduced pathological arterial neointima formation in vivo. In contrast, we observed little significant effect of SMC-specific Nrp1 knockout on neonatal retinal vascularization. Our results point to a requirement of Nrp1 in vascular smooth muscle and myofibroblast function in vivo, which may have relevance for postnatal lung development and for pathologies characterized by excessive SMC and/or myofibroblast proliferation.

Journal articles on the topic 'Retinal vascular remodeling'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles