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Journal articles on the topic 'Epithelium'
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1
Jin, Shiying. "Bipotent stem cells support the cyclical regeneration of endometrial epithelium of the murine uterus." Proceedings of the National Academy of Sciences 116, no. 14 (March 14, 2019): 6848–57. http://dx.doi.org/10.1073/pnas.1814597116.
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The endometrial epithelium of the uterus regenerates periodically. The cellular source of newly regenerated endometrial epithelia during a mouse estrous cycle or a human menstrual cycle is presently unknown. Here, I have used single-cell lineage tracing in the whole mouse uterus to demonstrate that epithelial stem cells exist in the mouse uterus. These uterine epithelial stem cells provide a resident cellular supply that fuels endometrial epithelial regeneration. They are able to survive cyclical uterine tissue loss and persistently generate all endometrial epithelial lineages, including the functionally distinct luminal and glandular epithelia, to maintain uterine cycling. The uterine epithelial stem cell population also supports the regeneration of uterine endometrial epithelium post parturition. The 5-ethynyl-2′-deoxyuridine pulse-chase experiments further reveal that this stem cell population may reside in the intersection zone between luminal and glandular epithelial compartments. This tissue distribution allows these bipotent uterine epithelial stem cells to bidirectionally differentiate to maintain homeostasis and regeneration of mouse endometrial epithelium under physiological conditions. Thus, uterine function over the reproductive lifespan of a mouse relies on stem cell-maintained rhythmic endometrial regeneration.
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Ramos, Tiago, Deborah Scott, and Sajjad Ahmad. "An Update on Ocular Surface Epithelial Stem Cells: Cornea and Conjunctiva." Stem Cells International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/601731.
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The human ocular surface (front surface of the eye) is formed by two different types of epithelia: the corneal epithelium centrally and the conjunctival epithelium that surrounds this. These two epithelia are maintained by different stem cell populations (limbal stem cells for the corneal epithelium and the conjunctival epithelial stem cells). In this review, we provide an update on our understanding of these epithelia and their stem cells systems, including embryology, new markers, and controversy around the location of these stem cells. We also provide an update on the translation of this understanding into clinical applications for the treatment of debilitating ocular surface diseases.
3
Kurokawa, I., S. Nishijima, K. Kusumoto, H. Senzaki, N. Shikata, and A. Tsubura. "Immunohistochemical Study of Cytokeratins in Hidradenitis Suppurativa (Acne Inversa)." Journal of International Medical Research 30, no. 2 (April 2002): 131–36. http://dx.doi.org/10.1177/147323000203000205.
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In 14 cases of hidradenitis suppurativa, cytokeratin (CK) expression was studied immunohistochemically, using six anti-keratin antibodies against CK1, CK10, CK14, CK16, CK17 and CK19, respectively. The draining sinus tract epithelium of hidradenitis suppurativa lesions was divided into three components: infundibular-like keratinized epithelium (type A), non-infundibular keratinized epithelium (type B), and non-keratinized epithelium (type C). In type A samples, CK17 (which is found in normal infundibulum) was not detected, suggesting fragility of this epithelial type. Keratin expression in types B and C epithelia was similar to that observed in the outer root sheath in normal hair follicles. Our results suggest that the draining sinus epithelium may possess characteristics of fragility, undifferentiation and hyperproliferation, as shown with CK expression.
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Ferguson, C. A., A. S. Tucker, and P. T. Sharpe. "Temporospatial cell interactions regulating mandibular and maxillary arch patterning." Development 127, no. 2 (January 15, 2000): 403–12. http://dx.doi.org/10.1242/dev.127.2.403.
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The cellular origin of the instructive information for hard tissue patterning of the jaws has been the subject of a long-standing controversy. Are the cranial neural crest cells prepatterned or does the epithelium pattern a developmentally uncommitted population of ectomesenchymal cells? In order to understand more about how orofacial patterning is controlled we have investigated the temporal signalling interactions and responses between epithelium and mesenchymal cells in the mandibular and maxillary primordia. We show that within the mandibular arch, homeobox genes that are expressed in different proximodistal spatial domains corresponding to presumptive molar and incisor ectomesenchymal cells are induced by signals from the oral epithelium. In mouse, prior to E10, all ectomesenchyme cells in the mandibular arch are equally responsive to epithelial signals such as Fgf8, indicating that there is no pre-specification of these cells into different populations and suggesting that patterning of the hard tissues of the mandible is instructed by the epithelium. By E10.5, ectomesenchymal cell gene expression domains are still dependent on epithelial signals but have become fixed and ectopic expression cannot be induced. At E11 expression becomes independent of epithelial signals such that removal of the epithelium does not affect spatial ectomesenchymal expression. Significantly, however, the response of ectomesenchyme cells to epithelial regulatory signals was found to be different in the mandibular and maxillary primordium. Thus, whereas both mandibular and maxillary arch epithelia could induce Dlx2 and Dlx5 expression in the mandible and Dlx2 expression in the maxilla, neither could induce Dlx5 expression in the maxilla. Reciprocal cell transplantations between mandibular and maxillary arch ectomesenchymal cells revealed intrinsic differences between these populations of cranial neural crest-derived cells. Research in odontogenesis has shown that the oral epithelium of the mandibular and maxillary primordia has unique instructive signaling properties required to direct odontogenesis, which are not found in other branchial arch epithelia. As a consequence, development of jaw-specific skeletal structures may require some prespecification of maxillary ectomesenchyme to restrict the instructive influence of the epithelial signals and allow development of maxillary structures distinct from mandibular structures.
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A, Suchetha, Anusha D, and Sapna Nadiger. "Epithelium - An Overview and an Insight on Gingival Epithelium: A Literature Review." International Journal of Research and Review 11, no. 1 (January 29, 2024): 538–53. http://dx.doi.org/10.52403/ijrr.20240160.
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Epithelium is comprised of cells that cover the exterior surfaces of the body and line both the internal closed cavities of the body and those that communicate with the exterior. The cells forming epithelium are in close apposition with one another, they may be arranged in multiple layers. In some locations cells are found aggregated in close apposition with one another but lack free surface. They are called epithelial like or epithelioid tissues. It is a tissue composed of a layer of cells which lines both the outside (skin) and the inside (e. g. intestine) of organisms. The epithelium serves as a barrier to protect the body from pathogens and functions to maintain homeostasis. In this review we will focus on organization and function of the epithelium with its distinctions among epithelia which includes fundamentals of organization, adhesion, polarity, and mechanical coordination and its role in oral mucous membrane. Keywords: Epithelium, cell junctions, gingival epithelium,basal lamina.
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Ferrante, S., T. Hackett, C. Hoptay, J. Engelhardt, J. Ingram, Y. Zhang, S. Alcala, et al. "9: AN IN VIVO MODEL OF HUMAN AIRWAYS FOR INVESTIGATING FIBROSIS." Journal of Investigative Medicine 64, no. 3 (February 25, 2016): 802.2–803. http://dx.doi.org/10.1136/jim-2016-000080.9.
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Purpose of StudyLimited models exist to investigate the airway epithelium's role in repair, regeneration, and pathology of chronic obstructive lung diseases. We introduce a human asthmatic airway epithelial xenograft system integrating a proliferating and differentiating airway epithelium with an actively remodeling rodent mesenchyme in an immunocompromised murine host. We hypothesized that epithelial regeneration in asthma induces underlying matrix fibrosis.Methods UsedHuman airway epithelial cells from asthmatic and non-asthmatic donors (n=5 per group) were seeded into decellularized rat tracheas. Tracheas were ligated to a sterile tubing cassette and implanted subcutaneously in the flanks of athymic nude mice. Grafts were harvested at 2, 4, or 6 weeks for analysis of tissue histology, fibrillar collagen deposition, and TGFβ1 activation. Non-transplantable human lungs from asthmatic and non-asthmatic donor FFPE sections were analyzed using similar methods.Summary of ResultsGrafted epithelial cells generated a differentiated epithelium with basal, ciliated, and mucus cells. By 4 weeks post-engraftment, asthmatic-derived epithelia showed decreased numbers of ciliated cells and E-cadherin expression compared to non-asthmatic controls, similar to human lung biopsy tissue. While there was no evidence of matrix remodeling in acellular xenografts, grafts seeded with asthmatic-derived epithelial cells had 3 times as much fibrillar collagen at 6 weeks post-engraftment as non-asthmatic epithelial seeded grafts. This was accompanied by a >2-fold induction of matrix TGFβ1 [with evidence of pSMAD3 activity] in asthmatic grafts at 4 weeks (positive pixels/total field pixels=0.12±0.001 vs. 0.05±0.001; p=0.003) and 6 weeks (0.09±0.02 vs. 0.04±0.01; p=0.044) post-engraftment.ConclusionsWe show in this model that asthmatic epithelium alone is sufficient to drive aberrant mesenchymal remodeling, specifically with fibrillar collagen deposition in asthmatic-derived xenografts.These xenografts are a major advance over current animal models of asthma in that they permit direct assessment of the epithelial-mesenchymal trophic unit.
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Yi, Jawoon, Harim Choi, Su-Man Kim, and Hyung-Sik Kang. "Deficiency of TAM receptor family increases γδT cell population by promoting chemokine-induced gut homing." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 84.10. http://dx.doi.org/10.4049/jimmunol.204.supp.84.10.
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Abstract Intestinal intraepithelial lymphocytes (IELs) are a various community of lymphoid cells located in between the intestinal epithelial cells (IECs) that configure the intestinal mucosal barrier. The epithelial γδT cells act as a major T cell population in epithelia, which is support in tissue homeostasis and repair. However, we found that the γδT cell population was strikingly increased in IELs in TAM receptor-deficient mice. Based on these data, we tested whether this receptor acts as a crucial regulator, which may generate better homing to the intestinal epithelium. We also tested that adoptive transfer of γδT cells to show γδT cell homing to the intestinal epithelium. Our study shows that a key factor in γδT cell homing into the intestinal epithelium, to maintain homeostasis.
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Oberst, Michael D., Baljit Singh, Metin Ozdemirli, Robert B. Dickson, Michael D. Johnson, and Chen-Yong Lin. "Characterization of Matriptase Expression in Normal Human Tissues." Journal of Histochemistry & Cytochemistry 51, no. 8 (August 2003): 1017–25. http://dx.doi.org/10.1177/002215540305100805.
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Matriptase is a type II transmembrane serine protease that has been implicated in the progression of epithelium-derived tumors. The role of this protease in the biology of normal epithelial cells remains to be elucidated. Matriptase mRNA has been detected by Northern analysis in tissues rich in epithelial cells, and the protein is expressed in vivo in normal and cancerous breast, ovarian, and colon tissues. However, a systematic analysis of the distribution of matriptase protein and mRNA in normal human tissues rich in epithelium has not been reported. In this study we characterized the expression of the protease in a wide variety of normal human tissues using a tissue microarray and whole tissue specimens. Significant immunoreactivity and mRNA expression were detected in the epithelial components of most epithelium-containing tissues. Matriptase expression was found in all types of epithelium, including columnar, pseudostratified columnar, cuboidal, and squamous. Distinct spatial distributions of reactivity were observed in the microanatomy of certain tissues, however. This suggests that although matriptase is broadly expressed among many types of epithelial cells, its activity within a tissue may be regulated in part at the protein and mRNA levels during the differentiation of selected epithelia.
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Burch, L. H., C. R. Talbot, M. R. Knowles, C. M. Canessa, B. C. Rossier, and R. C. Boucher. "Relative expression of the human epithelial Na+ channel subunits in normal and cystic fibrosis airways." American Journal of Physiology-Cell Physiology 269, no. 2 (August 1, 1995): C511—C518. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c511.
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The availability of the newly cloned subunits (alpha, beta, gamma) of the epithelial Na+ channel (ENaC) permits molecular studies of the pathogenesis of the abnormal Na+ transport rates of cystic fibrosis (CF) airway epithelia. Northern analyses of airway epithelia showed that both normal and CF airway epithelia express ENaC subunit mRNAs in a ratio of alpha > beta > gamma. In situ hybridization studies revealed expression of all three ENaC subunits in the superficial epithelium and the alpha- and beta-subunits in the gland ductular and acinar epithelium of both normal and CF airways. Ribonuclease protection assays revealed that the steady-state levels of alpha-, beta-, and gamma-ENaC mRNAs were similar in CF and normal airway superficial epithelia. These findings indicate that 1) Na+ transport defects in CF airways disease may be expressed in glandular acinar and ductal epithelium as well as superficial epithelium, and 2) the molecular pathogenesis of Na+ hyperabsorption in CF airways does not reflect increased levels of Na+ channel mRNAs, and probably number, but reflects an absence of the normal inhibitory regulation of Na+ channels by CF transmembrane conductance regulator proteins.
10
Parkos, Charles A. "I. Neutrophil adhesive interactions with intestinal epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 4 (October 1, 1997): G763—G768. http://dx.doi.org/10.1152/ajpgi.1997.273.4.g763.
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In many inflammatory conditions of the gastrointestinal tract, disease activity and patient symptoms correlate with the histological finding of neutrophil (PMN) migration across the epithelium. PMN interactions with intestinal epithelium can influence epithelial functions ranging from barrier maintenance to electrolyte secretion. Additionally, PMN recruitment to the epithelium can be modulated by epithelial interactions with luminal enteric pathogens. Adhesive interactions between PMN and intestinal epithelial cells have been shown to be distinct from interactions of PMN with endothelia. In particular, PMN transepithelial migration is modulated by a distinct array of cytokines including interferon-γ and interleukin-4 and requires the PMN β2-integrin CD11b/CD18 but is independent of CD11a/CD18, selectins, and intercellular adhesion molecule 1. Additionally, an integral membrane protein termed CD47 has recently been shown to play an important role in PMN transepithelial migration at point(s) subsequent to initial adhesive interactions. This article provides a brief overview of PMN interactions with epithelia and their functional consequences in relation to inflammatory disease.
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Maharshak, Nitsan, Eun Young Huh, Chorlada Paiboonrungruang, Michael Shanahan, Lance Thurlow, Jeremy Herzog, Zorka Djukic, et al. "Enterococcus faecalis Gelatinase Mediates Intestinal Permeability via Protease-Activated Receptor 2." Infection and Immunity 83, no. 7 (April 27, 2015): 2762–70. http://dx.doi.org/10.1128/iai.00425-15.
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Microbial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a dysbiotic enteric microbiota can lead to disease. This mechanism was investigated using the colitogenic, protease-secreting enteric microbeEnterococcus faecalis. Caco-2 and T-84 epithelial cell monolayers and the mouse colonic epithelium were exposed to concentrated conditioned media (CCM) fromE. faecalisV583 andE. faecalislacking the gelatinase gene (gelE). The flux of fluorescein isothiocyanate (FITC)-labeled dextran across monolayers or the mouse epithelium following exposure to CCM from parental or mutantE. faecalisstrains indicated paracellular permeability. A protease-activated receptor 2 (PAR2) antagonist and PAR2-deficient (PAR2−/−) mice were used to investigate the role of this receptor inE. faecalis-induced permeability. Gelatinase (GelE) purified fromE. faecalisV583 was used to confirm the ability of this protease to induce epithelial cell permeability and activate PAR2. The protease-mediated permeability of colonic epithelia from wild-type (WT) and PAR2−/−mice by fecal supernatants from ulcerative colitis patients was assessed. SecretedE. faecalisproteins induced permeability in epithelial cell monolayers, which was reduced in the absence ofgelEor by blocking PAR2 activity. SecretedE. faecalisproteins induced permeability in the colonic epithelia of WT mice that was absent in tissues from PAR2−/−mice. Purified GelE confirmed the ability of this protease to induce epithelial cell permeability via PAR2 activation. Fecal supernatants from ulcerative colitis patients induced permeability in the colonic epithelia of WT mice that was reduced in tissues from PAR2−/−mice. Our investigations demonstrate that GelE fromE. faecaliscan regulate enteric epithelial permeability via PAR2.
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Muggeo, Anaëlle, Christelle Coraux, and Thomas Guillard. "Current concepts on Pseudomonas aeruginosa interaction with human airway epithelium." PLOS Pathogens 19, no. 3 (March 30, 2023): e1011221. http://dx.doi.org/10.1371/journal.ppat.1011221.
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Pseudomonas aeruginosa is a major, but opportunistic, respiratory pathogen, which rarely infects healthy individuals, mainly due to the barrier effect of the human airway epithelium (HAE). This review explores the interaction of P. aeruginosa with HAE and the progression of the infection. The basolateral part of the epithelium, which includes the basolateral membrane of the epithelial cells and the basement membrane, is inaccessible in normal tight epithelia with intact junctions. We highlight how P. aeruginosa exploits weaknesses in the HAE barrier to gain access to the basolateral part of the epithelium. This access is crucial to initiate respiratory infection and is mainly observed in the injured epithelium, in repairing or chronically remodeled epithelium, and during extrusion of senescent cells or cell multiplication during normal epithelium renewal. The subsequent adhesion of the bacteria and cytotoxic action of virulence factors, including the toxins delivered by the type 3 secretion system (T3SS), lead to retractions and cell death. Eventually, P. aeruginosa progressively reaches the basement membrane and propagates radially through the basal part of the epithelium to disseminate using twitching and flagellar motility.
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Lin, Y., L. Xia, J. D. Turner, and X. Zhao. "Morphologic observation of neutrophil diapedesis across bovine mammary gland epithelium in vitro." American Journal of Veterinary Research 56, no. 2 (February 1, 1995): 203–7. http://dx.doi.org/10.2460/ajvr.1995.56.02.203.
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SUMMARY Neutrophils are present in milk of cows as a means of suppressing invading pathogens during mastitis. However, the manner by which neutrophils traverse the secretory epithelia is still not clear: do they diapedese between epithelial cells or do they kill epithelial cells to gain entry into milk? We investigated the process of bovine neutrophil diapedesis across bovine mammary gland epithelium in vitro. The bovine mammary epithelial cell line mac-t, grown on collagen-coated filters, formed a confluent monolayer with characteristic tight junctions, basal-apical polarity, and functional barriers to the dye trypan blue. Neutrophils added on the apical surface of the monolayer were stimulated to diapedese across the epithelium by the addition of Staphylococcus aureus (107 colony-forming units/ml) to the basal compartment. Light and transmission electron microscopy revealed the series of events for neutrophil transmigration: accumulation of neutrophils on the surface of epithelial monolayer; projection of pseudopods into intercellular junctions and movement of neutrophils between adjacent epithelial cells; and reapproximation of the lateral epithelial cell membranes and reformation of the apical tight junctions after neutrophils crossed the epithelium. Morphologically, epithelial cell damage caused by neutrophil diapedesis was not evident. This in vitro model provides a two-dimensional epithelial sheet by which neutrophil diapedesis can be qualitatively studied under defined conditions. Results of the study suggest a major mode by which bovine neutrophils diapedese across the alveolar epithelia into milk during mastitis.
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Ghosh, Saroj Kumar. "Histology and surface morphology of the olfactory epithelium in the freshwater teleost Clupisoma garua (Hamilton, 1822)." Fisheries & Aquatic Life 27, no. 3 (September 1, 2019): 122–29. http://dx.doi.org/10.2478/aopf-2019-0014.
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Abstract The anatomical structure of the olfactory organ and the organization of various cells lining the olfactory mucosa of Clupisoma garua (Siluriformes; Schilbeidae) were investigated with light and scanning electron microscopy. The olfactory organ was composed of numerous lamellae of various sizes, radiating outward from both sides of the narrow midline raphe, forming an elongated rosette. Each lamella consisted of the olfactory epithelium and a central lamellar space, the central core. The epithelium covering the surface of the rosette folds was differentiated into zones of sensory and indifferent epithelia. The sensory part of epithelium was characterized by three types of morphologically distinct receptor neurons: ciliated receptor cells, microvillous receptor cells, and rod receptor cells for receiving olfactory sensation from the aquatic environment. The indifferent epithelium comprising a large surface area of the lamella, was covered with compact non-sensory cilia. The non-sensory epithelium contained stratified epithelial cells with microridges, mucin secreting mucous cells, labyrinth cells, and basal cells, which were arranged in a layer at the base of the epithelium. Various cells on the olfactory epithelium were correlated with the functional significance of the fish concerned.
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Niklaus, Andrea L., and Jeffrey W. Pollard. "Mining the Mouse Transcriptome of Receptive Endometrium Reveals Distinct Molecular Signatures for the Luminal and Glandular Epithelium." Endocrinology 147, no. 7 (July 1, 2006): 3375–90. http://dx.doi.org/10.1210/en.2005-1665.
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Epithelia coat most tissues where they sense and respond to the environment and participate in innate immune responses. In the adult mouse uterus, columnar epithelium lines the central lumen and the glands that penetrate the underlying stroma. A nidatory surge of estrogen causes differentiation of the luminal epithelium to the receptive state that permits blastocyst attachment and allows subsequent implantation. Here, using laser-capture microdissection to isolate the luminal and glandular epithelia separately, we have profiled gene expression 2 h before embryo attachment to determine whether there are unique roles for these two epithelial structures in this process. Although most genes were expressed in both compartments, there was greater expression of 153 and 118 genes in the lumen and glands, respectively. In the luminal epithelium, there is enrichment in lipid, metal-ion binding, and carbohydrate-metabolizing enzymes, whereas in the glands, immune response genes are emphasized. In situ hybridization to uterine sections obtained from mice during the preimplantation period validated these data and indicated an array of previously undocumented genes expressed with unique patterns in these epithelia. The data show that each epithelial compartment has a distinct molecular signature and that they act differentially and synergistically to permit blastocyst implantation.
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Donjacour, A. A., and G. R. Cunha. "Induction of prostatic morphology and secretion in urothelium by seminal vesicle mesenchyme." Development 121, no. 7 (July 1, 1995): 2199–207. http://dx.doi.org/10.1242/dev.121.7.2199.
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Mesenchymal-epithelial interactions are essential for the development of the male reproductive tract. Tissue recombination experiments have been used to define the characteristics of these interactions. When mesenchyme, embryonic connective tissue, is recombined with epithelium from another organ an instructive induction may occur in which the developmental fate of the epithelium is altered. Instructive inductions are most common when the epithelium that is removed from the mesenchyme and the epithelium that is recombined with the mesenchyme are from the same germ layer. All of the mesenchyme of the male reproductive tract is of mesodermal origin. The epithelia of these organs are derived from either the mesodermal Wolffian duct epithelium or the endodermal urogenital sinus epithelium. Urogenital sinus mesenchyme can instructively induce bladder and urethral epithelium to form prostate (Donjacour, A. A. and Cunha, G. R. (1993) Endocrinol. 132, 2342–2350) and seminal vesicle mesenchyme can instructively induce epithelium from the ductus deferens and ureter (Cunha, G. R., Young, P., Higgins, S. J. and Cooke, P. S. (1991) Development 111, 145–158) to form seminal vesicle. To see whether inductive interactions could occur across germ layers in this system, seminal vesicle mesenchyme, normally associated with a mesodermal epithelium, was recombined with epithelium from neonatal or adult bladder or urethra, which are of endodermal origin. The resulting tissue recombinants were analyzed histologically and by immunocytochemistry and western blotting with antibodies to prostatic and seminal vesicle secretory proteins. Full prostatic differentiation was observed in tissue recombinants made with seminal vesicle mesenchyme plus either adult or neonatal bladder or urethral epithelium.(ABSTRACT TRUNCATED AT 250 WORDS)
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Davidson, Donald J., Fiona M. Kilanowski, Scott H. Randell, David N. Sheppard, and Julia R. Dorin. "A primary culture model of differentiated murine tracheal epithelium." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 4 (October 1, 2000): L766—L778. http://dx.doi.org/10.1152/ajplung.2000.279.4.l766.
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The goal of this study was to develop a primary culture model of differentiated murine tracheal epithelium. When grown on semipermeable membranes at an air interface, dissociated murine tracheal epithelial cells formed confluent polarized epithelia with high transepithelial resistances (∼12 kΩ · cm2) that remained viable for up to 80 days. Immunohistochemistry and light and electron microscopy demonstrated that the cells were epithelial in nature (cytokeratin positive, vimentin and α-smooth muscle actin negative) and differentiated to form ciliated and secretory cells from day 8 after seeding onward. With RT-PCR, expression of the cystic fibrosis transmembrane conductance regulator ( Cftr) and murine β-defensin ( Defb) genes was detected ( Defb-1 was constitutively expressed, whereas Defb-2 expression was induced by exposure to lipopolysaccharide). Finally, Ussing chamber experiments demonstrated an electrophysiological profile compatible with functional amiloride-sensitive sodium channels and cAMP-stimulated CFTR chloride channels. These data indicate that primary cultures of murine tracheal epithelium have many characteristics similar to those of murine tracheal epithelium in vivo. This method will facilitate the establishment of primary cultures of airway epithelium from transgenic mouse models of human diseases.
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Regauer, S., W. W. Franke, and I. Virtanen. "Intermediate filament cytoskeleton of amnion epithelium and cultured amnion epithelial cells: expression of epidermal cytokeratins in cells of a simple epithelium." Journal of Cell Biology 100, no. 4 (April 1, 1985): 997–1009. http://dx.doi.org/10.1083/jcb.100.4.997.
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Using immunofluorescence microscopy and two-dimensional gel electrophoresis, we compared the cytoskeletal proteins expressed by human amnion epithelium in situ, obtained from pregnancies of from 10-wk to birth, with the corresponding proteins from cultured amnion epithelial cells and cultures of cells from the amniotic fluid of 16 week pregnancies. Epithelia of week 16 fetuses already display tissue-specific patterns of cytokeratin polypeptides which are similar, although not identical, to those of the corresponding adult tissues. In the case of the simple amnion epithelium, a complex and characteristic complement of cytokeratin polypeptides of Mr 58,000 (No. 5), 56,000 (No. 6), 54,000 (No. 7), 52,500 (No. 8), 50,000 (No. 14), 46,000 (No. 17), 45,000 (No. 18), and 40,000 (No. 19) is present by week 10 of pregnancy and is essentially maintained until birth, with the addition of cytokeratin No. 4 (Mr 59,000) and the disappearance of No. 7 (Mr 54,000) at week 16 of pregnancy. In full-term placentae, the amnion epithelium displays two morphologically distinct regions, i.e., a simple and a stratified epithelium, both of which express the typical amnion cytokeratin polypeptides. However, in addition the stratified epithelium also synthesizes large amounts of special epidermal cytokeratins such as No. 1 (Mr 68,000), 10 (Mr 56,500), and 11 (Mr 56,000). In culture amnion epithelial cells obtained from either 16-wk pregnancies or full-term placentae will continue to synthesize the amnion-typical cytokeratin pattern, except for a loss of detection of component No. 4. This pattern is considerably different from the cytokeratins synthesized by cultures of cells from amniotic fluids (cytokeratins No. 7, 8, 18, and 19, sometimes with trace amounts of No. 17) and from several so-called "amnion epithelial cell lines." In addition, amnion epithelial cells in situ as well as amnion epithelial cell cultures appear to be heterogeneous in that they possess some cells that co-express cytokeratins and vimentin. These observations lead to several important conclusions: In contrast to the general concept of recent literature, positively charged cytokeratins of the group No. 4-6 can be synthesized in a simple, i.e., one-layered epithelium. The change from simple to stratified amnion epithelium does not require a cessation of synthesis of cytokeratins of the simple epithelium type, but in this case keratins characteristic of the terminally differentiated epidermis (No. 1, 10, and 11) are also synthesized.(ABSTRACT TRUNCATED AT 400 WORDS)
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Higgins, S. J., P. Young, and G. R. Cunha. "Induction of functional cytodifferentiation in the epithelium of tissue recombinants. II. Instructive induction of Wolffian duct epithelia by neonatal seminal vesicle mesenchyme." Development 106, no. 2 (June 1, 1989): 235–50. http://dx.doi.org/10.1242/dev.106.2.235.
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When grown as renal grafts in adult male hosts, the upper (cranial), middle and lower (caudal) portions of fetal mouse and rat Wolffian ducts developed into epididymis, epididymis plus ductus deferens, and seminal vesicle, respectively. In heterotypic tissue recombinants, the epithelia from upper and middle Wolffian ducts were instructively induced to undergo seminal vesicle morphogenesis by neonatal seminal vesicle mesenchyme. Functional cytodifferentiation was examined in these recombinants using antibodies against major androgen-dependent, seminal vesicle-specific secretory proteins. The instructively induced Wolffian duct epithelia synthesized normal amounts of all of the secretory proteins characteristic of mature seminal vesicles, as judged by immunocytochemistry on tissue sections and gel electrophoresis plus immunoblotting of secretions extracted from the recombinants. In heterospecific recombinants composed of rat and mouse tissues, the seminal vesicle proteins induced were specific for the species that had provided the epithelium. This showed that the seminal vesicle epithelium in the recombinants was derived from instructively induced Wolffian duct epithelium and not from epithelial contamination of the mesenchymal inductor. Upper Wolffian duct epithelium, instructively induced to undergo seminal vesicle morphogenesis, did not express epididymis-specific secretory proteins, showing that its normal development had been simultaneously repressed.
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Rochelle, Lori G., Dong Chen Li, Helen Ye, Eddie Lee, Colleen R. Talbot, and Richard C. Boucher. "Distribution of ion transport mRNAs throughout murine nose and lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 1 (July 1, 2000): L14—L24. http://dx.doi.org/10.1152/ajplung.2000.279.1.l14.
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Evidence of absorptive or secretory ion transport in different respiratory regions of the mouse was sought by assessing the regional distribution of α-, β-, and γ-epithelial sodium channel (ENaC; Na+ absorptive), cystic fibrosis transmembrane conductor regulator (CFTR), and Na+-K+-2Cl− cotransporter mRNAs. High levels of ENaC subunit expression were found in nasal surface epithelium and gland ducts. CFTR was expressed in both superficial nasal respiratory epithelium and glands. These results are consistent with basal amiloride-sensitive Na+ absorption and cAMP-dependent Cl− secretion in murine nasal epithelia. Expression of all three ENaC subunits increased progressively from trachea to terminal bronchioles. Intermediate levels of CFTR and cotransporter expression in bronchial epithelium diminished in bronchioles. The low abundance of CFTR mRNA throughout murine pulmonary epithelium is consistent with functional data that attributes Cl− secretion predominantly to an alternative Cl− channel. α-ENaC as the only mRNA found in all regions of airway epithelia is consistent with the α-subunit as requisite for Na+ absorption, and the increased expression of α-, β-, and γ-ENaC in distal airways suggests a greater absorptive capability in this region.
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Gerbe, François, Johan H. van Es, Leila Makrini, Bénédicte Brulin, Georg Mellitzer, Sylvie Robine, Béatrice Romagnolo, et al. "Distinct ATOH1 and Neurog3 requirements define tuft cells as a new secretory cell type in the intestinal epithelium." Journal of Cell Biology 192, no. 5 (March 7, 2011): 767–80. http://dx.doi.org/10.1083/jcb.201010127.
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The unique morphology of tuft cells was first revealed by electron microscopy analyses in several endoderm-derived epithelia. Here, we explore the relationship of these cells with the other cell types of the intestinal epithelium and describe the first marker signature allowing their unambiguous identification. We demonstrate that although mature tuft cells express DCLK1, a putative marker of quiescent stem cells, they are post-mitotic, short lived, derive from Lgr5-expressing epithelial stem cells, and are found in mouse and human tumors. We show that whereas the ATOH1/MATH1 transcription factor is essential for their differentiation, Neurog3, SOX9, GFI1, and SPDEF are dispensable, which distinguishes these cells from enteroendocrine, Paneth, and goblet cells, and raises from three to four the number of secretory cell types in the intestinal epithelium. Moreover, we show that tuft cells are the main source of endogenous intestinal opioids and are the only epithelial cells that express cyclooxygenase enzymes, suggesting important roles for these cells in the intestinal epithelium physiopathology.
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AL-Medhtiy, Morteta H. Mohamed. "Histological Study of the Larynxinindigenous male WestAfrican guinea fowl (Numidameleagrisgaleata)In AL-Najaf province." Kufa Journal For Veterinary Medical Sciences 5, no. 2 (December 31, 2014): 332–39. http://dx.doi.org/10.36326/kjvs/2014/v5i24175.
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Microscopic investigation of the larynx in Indigenous Male West African guinea fowl (Numida meleagris galeata) In AL-Najaf province, the mean live weight was (1750 g ± 50 gm) our need to have a base line data on the respiratory system of this abundant species of bird in Iraq. It is expected that this work will provide a base for future research and subsequent clinical application as regards the biology of the guinea fowl. Five healthy birds utilize in this study. After bird dead the larynx dissected out and washing by normal saline solution, then were fixed immediately in 10% NBF solution, and then preparing for routine histological processing. The laryngeal mound was covered by non-keratinized stratified squamous epithelium. Toward the glottis the thickness of these epithelia decreased and some of epithelial layers were modified to epithelial glands, then epithelium became ciliated, pseudostratified columnar epithelium. Lamina propria-submucosa contained loose connective tissue connected with the perichondrium of the hyaline laryngeal cartilages (Cricoid, Arytenoid, and Procricoid).
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McDonald, Keely, Leroy Wheeler, Jeremiah McDole, Mark Miller, and Rodney Newberry. "CCR6 expression by small intestine lamina propria dendritic cells is critical for surveillance of the luminal contents at the villous epithelial surface (CCR5P.251)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 181.5. http://dx.doi.org/10.4049/jimmunol.192.supp.181.5.
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Abstract The immune system underlying the villous epithelium is continually monitoring its complex environment to appropriately respond with the induction of tolerance or immunity. However little is known about the factors promoting immune surveillance of the luminal contents at this surface. Mice deficient in lymphotoxin beta receptor (LTBR) have a decreased population of dendritic cells (DCs) associated with the villous epithelium. The chemokine CCL20 is expressed by the villous epithelium in a LTBR dependent manner, and CCR6, the only receptor for CCL20, is expressed by the LP-DCs associating with the villous epithelium. Using an in vivo imaging approach, we observed that LP-DC from CCR6 deficient mice were further from the intestinal lumen and flow cytometric analysis revealed they had a decreased population of epithelia associated LP-DCs. Mixed bone marrow transfers confirmed that CCR6 expression by DCs was required for association with the epithelium. In vivo imaging and flow cytometry revealed that LP-DCs from CCR6-/- mice were not impaired at migrating in the lymphatics or populating the mesenteric lymph node. However LP-DCs from CCR6-/- mice were deficient at acquiring epithelial cell proteins and intraluminal ovalbumin, and were deficient in priming immune responses to luminal antigen in the mesenteric lymph nodes. These findings identify an essential role for CCR6 expression by LP-DCs in surveillance of the luminal environment at the villous epithelial surface.
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Hirano, Akikazu, Kenshi Yao, Hiroshi Ishihara, Takashi Hisabe, Kentaro Imamura, Takao Kanemitsu, Kensei Ohtsu, et al. "Nature of a white opaque substance visualized by magnifying endoscopy in colorectal hyperplastic polyps." Endoscopy International Open 09, no. 07 (June 17, 2021): E1077—E1083. http://dx.doi.org/10.1055/a-1452-9669.
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Abstract Background and study aims A white opaque substance (WOS) has been observed in the epithelia of gastric, duodenal, and colorectal epithelial adenomas and carcinomas, using magnifying endoscopy (ME). The WOS has been reported to be derived from a dense accumulation of minute lipid droplets in the epithelium. This study aimed to investigate whether the WOS in colorectal hyperplastic polyps was derived from lipid droplets accumulated in the epithelium, as observed in the case of gastric, duodenal, and colorectal epithelial neoplasms. Patients and methods We analyzed 30 consecutive patients who were positive for the WOS, as visualized in colorectal hyperplastic polyps by ME with narrow-band imaging and 30 consecutive patients who were negative for the WOS. Biopsy specimens obtained from the polyps were immunostained with anti-adipophilin antibody to determine the correlation between the presence of the WOS and that of lipid droplets in the epithelium. Results In all patients, the epithelial cells were histologically positive for adipophilin. However, the area of adipophilin-positive epithelial cells in the WOS-positive group was significantly larger than that in the WOS-negative group (P < 0.001). The density of the WOS was strongly and positively correlated with the area of adipophilin-positive cells. Conclusions This study reveals that the WOS visualized in the superficial layers of colorectal hyperplastic polyps is produced by a dense accumulation of minute lipid droplets in the epithelia of the polyps.
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Sweat, Y. Y., M. Sweat, W. Yu, M. Sanz-Navarro, L. Zhang, Z. Sun, S. Eliason, et al. "Sox2 Controls Periderm and Rugae Development to Inhibit Oral Adhesions." Journal of Dental Research 99, no. 12 (July 17, 2020): 1397–405. http://dx.doi.org/10.1177/0022034520939013.
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In humans, ankyloglossia and cleft palate are common congenital craniofacial anomalies, and these are regulated by a complex gene regulatory network. Understanding the genetic underpinnings of ankyloglossia and cleft palate will be an important step toward rational treatment of these complex anomalies. We inactivated the Sry (sex-determining region Y)–box 2 ( Sox2) gene in the developing oral epithelium, including the periderm, a transient structure that prevents abnormal oral adhesions during development. This resulted in ankyloglossia and cleft palate with 100% penetrance in embryos examined after embryonic day 14.5. In Sox2 conditional knockout embryos, the oral epithelium failed to differentiate, as demonstrated by the lack of keratin 6, a marker of the periderm. Further examination revealed that the adhesion of the tongue and mandible expressed the epithelial markers E-Cad and P63. The expanded epithelia are Sox9-, Pitx2-, and Tbx1-positive cells, which are markers of the dental epithelium; thus, the dental epithelium contributes to the development of oral adhesions. Furthermore, we found that Sox2 is required for palatal shelf extension, as well as for the formation of palatal rugae, which are signaling centers that regulate palatogenesis. In conclusion, the deletion of Sox2 in oral epithelium disrupts palatal shelf extension, palatal rugae formation, tooth development, and periderm formation. The periderm is required to inhibit oral adhesions and ankyloglossia, which is regulated by Sox2. In addition, oral adhesions occur through an expanded dental epithelial layer that inhibits epithelial invagination and incisor development. This process may contribute to dental anomalies due to ankyloglossia.
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Bakhtin, A. A., and E. L. Tumanova. "Cytokeratin expression in reactive cylindrical ciliated epithelium of the sinonasal tract in chronic inflammation." CLINICAL AND EXPERIMENTAL MORPHOLOGY 12, no. 2 (2022): 14–24. http://dx.doi.org/10.31088/cem2023.12.2.14-24.
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Introduction. Currently, there are limited papers on changes in the pseudostratified ciliated columnar epithelium of the sinonasal tract in chronic inflammatory processes, particularly in basal cell hyperplasia. The latter is similar to dysplasia of varying severity of the stratified squamous nonkeratinized epithelium. Studying of changes in the pseudostratified ciliated columnar epithelium can clarify the histogenesis of various epithelial tumors of the sinonasal tract, including sinonasal papillomas. The research is aimed at studying the cytokeratin profile of reactive cylindrical ciliated epithelium in a chronic nonspecific inflammatory process. Materials and methods. We analyzed surgical materials obtained from 567 patients diagnosed with chronic rhinosinusitis with nasal polyps. We performed an immunohistochemical study in 20 cases using the panel of antibodies to Ki-67, Stathmin, Cytokeratin 7, Cytokeratin 10/13, Cytokeratin 14, Cytokeratin 17, Cytokeratin 18, and Cytokeratin 19. Results. Using hematoxylin and eosin staining, we detected basal cell hyperplasia of different severity in 74% (419 cases). In 13% (73 cases), basal cell hyperplasia was combined with foci of squamous metaplasia. Based on the results, we identified 4 types of morphological changes in the epithelial layer with a specific cytokeratin profile: mild basal cell hyperplasia, moderate basal cell hyperplasia, severe basal cell hyperplasia, and areas of squamous metaplasia. Conclusion. Simultaneous expression of cytokeratins in the areas with severe hyperplasia of basal cells, specific for both simple and compound epithelia, allows us to consider this area to have the highest potential for the development of various epithelial tumors of the sinonasal tract, including various types of sinonasal papillomas. Keywords: basal cell hyperplasia, sinonasal papilloma, pseudostratified columnar ciliated epithelium
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Bosshardt, D. D., and N. P. Lang. "The Junctional Epithelium: from Health to Disease." Journal of Dental Research 84, no. 1 (January 2005): 9–20. http://dx.doi.org/10.1177/154405910508400102.
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The junctional epithelium is located at a strategically important interface between the gingival sulcus, populated with bacteria, and the periodontal soft and mineralized connective tissues that need protection from becoming exposed to bacteria and their products. Its unique structural and functional adaptation enables the junctional epithelium to control the constant microbiological challenge. The antimicrobial defense mechanisms of the junctional epithelium, however, do not preclude the development of gingival and periodontal lesions. The conversion of the junctional to pocket epithelium, which is regarded as a hallmark in disease initiation, has been the focus of intense research in recent years. Research has shown that the junctional epithelial cells may play a much more active role in the innate defense mechanisms than previously assumed. They synthesize a variety of molecules directly involved in the combat against bacteria and their products. In addition, they express molecules that mediate the migration of polymorphonuclear leukocytes toward the bottom of the gingival sulcus. Periodontopathogens—such as Actinobacillus actinomycetemcomitans or, in particular, Porphyromonas gingivalis—have developed sophisticated methods to perturb the structural and functional integrity of the junctional epithelium. Research has focused on the direct effects of gingipains, cysteine proteinases produced by Porphyromonas gingivalis, on junctional epithelial cells. These virulence factors may specifically degrade components of the cell-to-cell contacts. This review will focus on the unique structural organization of the junctional epithelium, on the nature and functions of the various molecules expressed by its cells, and on how gingipains may attenuate the junctional epithelium’s structural and functional integrity.
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Clemons, Nicholas J., David H. Wang, Daniel Croagh, Anjali Tikoo, Christina M. Fennell, Carmel Murone, Andrew M. Scott, D. Neil Watkins, and Wayne A. Phillips. "Sox9 drives columnar differentiation of esophageal squamous epithelium: a possible role in the pathogenesis of Barrett's esophagus." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 12 (December 15, 2012): G1335—G1346. http://dx.doi.org/10.1152/ajpgi.00291.2012.
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The molecular mechanism underlying the development of Barrett's esophagus (BE), the precursor to esophageal adenocarcinoma, remains unknown. Our previous work implicated sonic hedgehog (Shh) signaling as a possible driver of BE and suggested that bone morphogenetic protein 4 (Bmp4) and Sox9 were downstream mediators. We have utilized a novel in vivo tissue reconstitution model to investigate the relative roles of Bmp4 and Sox9 in driving metaplasia. Epithelia reconstituted from squamous epithelial cells or empty vector-transduced cells had a stratified squamous phenotype, reminiscent of normal esophagus. Expression of Bmp4 in the stromal compartment activated signaling in the epithelium but did not alter the squamous phenotype. In contrast, expression of Sox9 in squamous epithelial cells induced formation of columnar-like epithelium with expression of the columnar differentiation marker cytokeratin 8 and the intestinal-specific glycoprotein A33. In patient tissue, A33 protein was expressed specifically in BE, but not in normal esophagus. Expression of Cdx2, another putative driver of BE, alone had no effect on reconstitution of a squamous epithelium. Furthermore, epithelium coexpressing Cdx2 and Sox9 had a phenotype similar to epithelium expressing Sox9 alone. Our results demonstrate that Sox9 is sufficient to drive columnar differentiation of squamous epithelium and expression of an intestinal differentiation marker, reminiscent of BE. These data suggest that Shh-mediated expression of Sox9 may be an important early event in the development of BE and that the potential for inhibitors of the hedgehog pathway to be used in the treatment of BE and/or esophageal adenocarcinoma could be tested in the near future.
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RICE, MICHAEL A., and GROVER C. STEPHENS. "Influx and Transepithelial Flux of Amino Acids in the Mussel, Mytilus Edulis." Journal of Experimental Biology 135, no. 1 (March 1, 1988): 275–87. http://dx.doi.org/10.1242/jeb.135.1.275.
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The uptake of amino acids by the non-gill epithelia of the mantle cavity of Mytilus edulis L. was studied and compared with uptake by the gills. Amino acid entry rates and the subsequent distribution of amino acids to the other tissues of the animals were studied using high-performance liquid chromatography and radiochemical techniques. Uptake via the non-gill epithelia lining the mantle cavity was separated from uptake via the gill by employing a preparation in which the gills were surgically removed. Amino acid uptake by such animals was compared with that of suitably sham-operated controls. In short-term experiments (up to 2h), transfer of substrate from the gills to other tissues of the animal is extremely limited. Amino acids taken up by the non-gill epithelia of the mantle cavity are rapidly transferred to deeper tissues. Roughly 25% of alpha-amino acids enter the animal via the non-gill epithelia. Estimates of total epithelial surface area for the gills and non-gill mantle epithelium are compared with entry rates of amino acid substrates via the two routes. The apparent densities of carriers for alanine and cycloleucine per unit area of surface are approximately equal for these two substrates. The density of taurine carriers per unit area of non-gill epithelium is apparently significantly higher than their density per unit area of gill epithelium. Finally, evidence is presented for differential sensitivity of taurine transporters in the non-gill epithelium to inhibition by alpha-amino acids.
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Mustonen, MV, MH Poutanen, S. Kellokumpu, Y. de Launoit, VV Isomaa, RK Vihko, and PT Vihko. "Mouse 17 beta-hydroxysteroid dehydrogenase type 2 mRNA is predominantly expressed in hepatocytes and in surface epithelial cells of the gastrointestinal and urinary tracts." Journal of Molecular Endocrinology 20, no. 1 (February 1, 1998): 67–74. http://dx.doi.org/10.1677/jme.0.0200067.
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17 beta-Hydroxysteroid dehydrogenase (17HSD) type 2 efficiently catalyzes the conversion of the high activity 17 beta-hydroxy forms of sex steroids into less potent 17-ketosteroids. In the present study in situ hybridization was utilized to analyze the cellular localization of 17HSD type 2 expression in adult male and female mice. The data indicate that 17HSD type 2 mRNA is expressed in several epithelial cell layers, including both absorptive and secretory epithelia as well as protective epithelium. In both males and females, strong expression of 17HSD type 2 was particularly detected in epithelial cells of the gastrointestinal and urinary tracts. The mRNA was expressed in the stratified squamous epithelium of the esophagus, and surface epithelial cells of the stomach, small intestine and colon. The hepatocytes of the liver and the thick limbs of the loops of Henle in the kidneys, as well as the epithelium of the urinary bladder, also showed strong expression of 17HSD type 2 mRNA in both male and female mice. In the genital tracts, low 17HSD type 2 expression was detected in the seminiferous tubules, the uterine epithelial cells and the surface epithelium of the ovary. Expression of the mRNA was also detected in the sebaceous glands of the skin. The results indicate that in both male and female mice, 17HSD type 2 is expressed mainly in the various epithelial cell types of the gastrointestinal and urinary tracts, and therefore suggest a role for the enzyme in steroid inactivation in a range of tissues and cell types not considered as classical sex steroid target tissues.
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Bosch, F. X., R. E. Leube, T. Achtstätter, R. Moll, and W. W. Franke. "Expression of simple epithelial type cytokeratins in stratified epithelia as detected by immunolocalization and hybridization in situ." Journal of Cell Biology 106, no. 5 (May 1, 1988): 1635–48. http://dx.doi.org/10.1083/jcb.106.5.1635.
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Multi-layered ("stratified") epithelia differ from one-layered ("simple") polar epithelia by various architectural and functional properties as well as by their cytoskeletal complements, notably a set of cytokeratins characteristic of stratified tissue. The simple epithelial cytokeratins 8 and 18 have so far not been detected in any stratified epithelium. Using specific monoclonal antibodies we have noted, in several but not all samples of stratified epithelia, including esophagus, tongue, exocervix, and vagina, positive immunocytochemical reactions for cytokeratins 8, 18, and 19 which in some regions were selective for the basal cell layer(s) but extended into suprabasal layers in others. In situ hybridization with different probes (riboprobes, synthetic oligonucleotides) for mRNAs of cytokeratin 8 on esophageal epithelium has shown, in extended regions, relatively strong reactivity for cytokeratin 8 mRNA in the basal cell layer. In contrast, probes to cytokeratin 18 have shown much weaker hybridization which, however, was rather evenly spread over basal and suprabasal strata. These results, which emphasize the importance of in situ hybridization in studies of gene expression in complex tissues, show that the genes encoding simple epithelial cytokeratins can be expressed in stratified epithelia. This suggests that continual expression of genes coding for simple epithelial cytokeratins is compatible with the formation of squamous stratified tissues and can occur, at least in basal cell layers, simultaneously with the synthesis of certain stratification-related cytokeratins. We also emphasize differences of expression and immunoreactivity of these cytokeratins between different samples and in different regions of the same stratified epithelium and discuss the results in relation to changes of cytokeratin expression during fetal development of stratified epithelia, in response to environmental factors and during the formation of squamous cell carcinomas.
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Greenburg, G., and E. D. Hay. "Cytoskeleton and thyroglobulin expression change during transformation of thyroid epithelium to mesenchyme-like cells." Development 102, no. 3 (March 1, 1988): 605–22. http://dx.doi.org/10.1242/dev.102.3.605.
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In considering the mechanism of transformation of epithelium to mesenchyme in the embryo, it is generally assumed that the ability to give rise to fibroblast-like cells is lost as epithelia mature. We reported previously that a definitive embryonic epithelium, that of the anterior lens, gives rise to freely migrating mesenchyme-like cells when suspended in type I collagen matrices. Here, we show that a highly differentiated epithelium that expresses cytokeratin changes to a vimentin cytoskeleton and loses thyroglobulin during epithelial-mesenchymal transformation induced by suspension in collagen gel. Using dispase and collagenase, we isolated adult thyroid follicles devoid of basal lamina and mesenchyme, and we suspended the follicles in 3D collagen gels. Cells bordering the follicle lumen retain epithelial polarity and thyroid phenotype, but basal cell surface organization is soon modified as a result of tissue multilayering and elongation of basal cells into the collagenous matrix. Cytodifferentiation, determined by thyroglobulin immunoreactivity, is lost as the basal epithelial cells move into the matrix after 3–4 days in collagen. By TEM, it can be seen that the elongating cells acquire pseudopodia, filopodia and mesenchyme-like nuclei and RER. Immunofluorescence examination of intermediate filaments showed that freshly isolated follicles and follicles cultured on planar substrata react only with anticytokeratin. However, all of the mesenchyme-like cells express vimentin and they gradually lose cytokeratin. These results suggest that vimentin may be necessary for cell functions associated with migration within a 3D matrix. The mesenchymal cells do not revert to epithelium when grown on planar substrata and the transformation of epithelium to mesenchyme-like cells does not occur within basement membrane gels. The results are relevant to our understanding of the initiation of epithelial-mesenchymal transformation in the embryo and the genetic mechanisms controlling cell shape, polarity and cytoskeletal phenotype.
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Hayman, Ian R., Rachel M. Temple, Cole K. Burgess, Mary Ferguson, Jason Liao, Craig Meyers, and Clare E. Sample. "New insight into Epstein-Barr Virus infection using models of stratified epithelium." PLOS Pathogens 19, no. 1 (January 11, 2023): e1011040. http://dx.doi.org/10.1371/journal.ppat.1011040.
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Epstein-Barr virus (EBV) is a ubiquitous human pathogen that is transmitted in saliva. EBV transits through the oral epithelium to infect B cells, where it establishes a life-long latent infection. Reinfection of the epithelium is believed to be mediated by virus shed from B cells, but whether a latent reservoir can exist in the epithelia is unknown. We previously developed an in vitro organotypic model of stratified epithelium where EBV can readily replicate within the suprabasal layers of the epithelium following apical infection mediated by virus-producing B cells. Given that infected epithelial cells and cell-free virus are observed in saliva, we examined the ability of both of these to mediate infection in organotypic cultures. Epithelial-derived cell-free virus was able to infect organotypic cultures from the apical surface, but showed enhanced infection of B cells. Conversely, B cell-derived virus exhibited enhanced infection of epithelial cells. While EBV has been detected in basal cells in oral hairy leukoplakia, it is unknown whether EBV can be seen in undifferentiated primary keratinocytes in the basal layer. Undifferentiated epithelial cells expressed proposed EBV receptors in monolayer and were susceptible to viral binding and entry. Integrins, and occasionally ephrin A2, were expressed in the basal layer of gingiva and tonsil derived organotypic cultures, but the known B-cell receptors HLAII and CD21 were not detected. Following infection with cell-free virus or virus-producing B cells at either the apical or basolateral surface of preformed organotypic cultures, abundant infection was detected in differentiated suprabasal cells while more limited but readily detectable infection was observed in the undifferentiated basal cells. Together, our data has provided new insight into EBV infection in stratified epithelium.
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Vermeer, Paola D., Lacey Panko, Philip Karp, John H. Lee, and Joseph Zabner. "Differentiation of human airway epithelia is dependent on erbB2." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 2 (August 2006): L175—L180. http://dx.doi.org/10.1152/ajplung.00547.2005.
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A clinical case documented a reversible change in airway epithelial differentiation that coincided with the initiation and discontinuation of trastuzumab, an anti-erbB2 antibody. This prompted the investigation into whether blocking the erbB2 receptor alters differentiation of the airway epithelium. To test this hypothesis, we treated an in vitro model of well-differentiated human airway epithelia with trastuzumab or heregulin-α, an erbB ligand. In addition, coculturing with human lung fibroblasts tested whether in vivo subepithelial fibroblasts function as an endogenous source of ligands able to activate erbB receptors expressed by the overlying epithelial cells. Epithelia were stained with hematoxylin and eosin and used for morphometric analysis. Trastuzumab treatment decreased the ciliated cell number by 49% and increased the metaplastic, flat cell number by 640%. Heregulin-α treatment increased epithelial height and decreased the number of metaplastic and nonciliated columnar cells, whereas it increased the goblet cell number. We found that normal human lung fibroblasts express transforming growth factor-α, heparin-binding epidermal-like growth factor, epiregulin, heregulin-α, and amphiregulin, all of which are erbB ligands. Cocultures of airway epithelia with primary fibroblasts increased epithelial height comparable to that achieved following heregulin-α treatment. These data show that erbB2 stimulation is required for maintaining epithelial differentiation. Furthermore, the mesenchyme underlying the airway epithelium secretes a variety of erbB ligands that may direct various pathways of epithelial differentiation.
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Kennel, Christopher, Elizabeth A. Gould, Eric D. Larson, Ernesto Salcedo, Thad Vickery, Diego Restrepo, and Vijay R. Ramakrishnan. "Differential Expression of Mucins in Murine Olfactory Versus Respiratory Epithelium." Chemical Senses 44, no. 7 (July 12, 2019): 511–21. http://dx.doi.org/10.1093/chemse/bjz046.
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Abstract Mucins are a key component of the surface mucus overlying airway epithelium. Given the different functions of the olfactory and respiratory epithelia, we hypothesized that mucins would be differentially expressed between these 2 areas. Secondarily, we evaluated for potential changes in mucin expression with radiation exposure, given the clinical observations of nasal dryness, altered mucus rheology, and smell loss in radiated patients. Immunofluorescence staining was performed to evaluate expression of mucins 1, 2, 5AC, and 5B in nasal respiratory and olfactory epithelia of control mice and 1 week after exposure to 8 Gy of radiation. Mucins 1, 5AC, and 5B exhibited differential expression patterns between olfactory and respiratory epithelium (RE) while mucin 2 showed no difference. In the olfactory epithelium (OE), mucin 1 was located in a lattice-like pattern around gaps corresponding to dendritic knobs of olfactory sensory neurons, whereas in RE it was intermittently expressed by surface goblet cells. Mucin 5AC was expressed by subepithelial glands in both epithelial types but to a higher degree in the OE. Mucin 5B was expressed by submucosal glands in OE and by surface epithelial cells in RE. At 1-week after exposure to single-dose 8 Gy of radiation, no qualitative effects were seen on mucin expression. Our findings demonstrate that murine OE and RE express mucins differently, and characteristic patterns of mucins 1, 5AC, and 5B can be used to define the underlying epithelium. Radiation (8 Gy) does not appear to affect mucin expression at 1 week. Level of Evidence N/A (Basic Science Research). IACUC-approved study [Protocol 200065].
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Shuler, Charles F. "Programmed Cell Death and Cell Transformation in Craniofacial Development." Critical Reviews in Oral Biology & Medicine 6, no. 3 (July 1995): 202–17. http://dx.doi.org/10.1177/10454411950060030301.
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Fusion of branchial arch derivatives is an essential component in the development of craniofacial structures. Bilaterally symmetric branchial arch processes fuse in the midline to form the mandible, lips, and palate. The mechanism for fusion requires several different morphologic and molecular events prior to the completion of the mesenchymal continuity between opposing tissue processes. The ectodermal covering of the branchial arches is one of the cell types that has an important role during craniofacial development. The surface epithelia provide the initial adherence between the processes; however, this population of cells is ultimately absent from the fusion zone. The medial edge epithelium of the secondary palatal shelves is one example of such an epithelium that must disappear from the fusion zone of the secondary palate during development in order to complete palatal fusion. The mechanisms for removal of the epithelial cells from the fusion zone could include either programmed cell death, epithelial-mesenchymal transformation, or migration to adjacent epithelia. All three of these fates have been hypothesized as a mechanism for the removal of the palatal medial edge epithelia. The processes of programmed cell death, epithelial-mesenchymal transformation, and epithelial migration are reviewed with respect to both palatal fusion and results reported in other model systems.
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Sun, D., C. R. Vanderburg, G. S. Odierna, and E. D. Hay. "TGFbeta3 promotes transformation of chicken palate medial edge epithelium to mesenchyme in vitro." Development 125, no. 1 (January 1, 1998): 95–105. http://dx.doi.org/10.1242/dev.125.1.95.
Full textAbstract:
Epithelial-mesenchymal transformation plays an important role in the disappearance of the midline line epithelial seam in rodent palate, leading to confluence of the palate. The aim of this study was to test the potential of the naturally cleft chicken palate to become confluent under the influence of growth factors, such as TGFbeta3, which are known to promote epithelial-mesenchymal transformation. After labeling medial edge epithelia with carboxyfluorescein, palatal shelves (E8-9) with or without beak were dissected and cultured on agar gels. TGFbeta1, TGFbeta2 or TGFbeta3 was added to the chemically defined medium. By 24 hours in culture, medial edge epithelia form adherent midline seams in all paired groups without intact beaks. After 72 hours, seams in the TGFbeta3 groups disappear and palates become confluent due to epithelial-mesenchymal transformation, while seams remain mainly epithelial in control, TGFbeta1 and TGFbeta2 groups. Epithelium-derived mesenchymal cells are identified by carboxyfluorescein fluorescence with confocal microscopy and by membrane-bound carboxyfluorescein isolation bodies with electron microscopy. Labeled fibroblasts completely replace the labeled epithelia of origin in TGFbeta3-treated palates without beaks. Single palates are unable to undergo transformation, and paired palatal shelves with intact beaks do not adhere or undergo transformation, even when treated with TGFbeta3. Thus, physical contact of medial edge epithelia and formation of the midline seam are necessary for epithelial-mesenchymal transformation to be triggered. We conclude that there may be no fundamental difference in developmental potential of the medial edge epithelium for transformation to mesenchyme among reptiles, birds and mammals. The bird differs from other amniotes in having developed a beak and associated craniofacial structures that seemingly keep palatal processes separated in vivo. Even control medial edge epithelia partly transform to mesenchyme if placed in close contact. However, exogenous TGFbeta3 is required to achieve complete confluence of the chicken palate.
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Clarke, L. L., and R. C. Boucher. "Chloride secretory response to extracellular ATP in human normal and cystic fibrosis nasal epithelia." American Journal of Physiology-Cell Physiology 263, no. 2 (August 1, 1992): C348—C356. http://dx.doi.org/10.1152/ajpcell.1992.263.2.c348.
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Chloride secretion across cystic fibrosis (CF) airway epithelia is effectively regulated by pathways associated with intracellular Ca2+ metabolism, but not by mechanisms dependent on protein kinase A or C. In a search for therapeutically useful agonists, we investigated the effects of extracellular ATP on the Cl- secretory process in human normal and CF nasal epithelial cultures with double-barreled Cl- selective microelectrodes. When applied to the basolateral membrane of normal, but not CF, nasal epithelium, extracellular ATP (10(-4) M) stimulated a small increase in Cl- secretion that was primarily associated with a hyperpolarizing conductance in the basolateral membrane. In contrast, ATP applied to the apical (luminal) membrane of either normal or CF nasal epithelium stimulated a greater increase in Cl- secretion that was associated with activation of an apical membrane Cl- conductance. The increases in Cl- current and apical conductance were greater in CF tissues and attained maximal values similar to normal nasal epithelium. We conclude 1) that basolateral application of ATP indirectly induces Cl- secretion by activating a basolateral (K+) conductance and is an effective secretagogue only in normal nasal epithelium and 2) that luminally applied ATP is an effective Cl- secretagogue that activates the apical membrane Cl- conductance of normal and CF nasal epithelia to an equivalent level.
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Munakata, M., I. Huang, W. Mitzner, and H. Menkes. "Protective role of epithelium in the guinea pig airway." Journal of Applied Physiology 66, no. 4 (April 1, 1989): 1547–52. http://dx.doi.org/10.1152/jappl.1989.66.4.1547.
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We developed an in vitro system to assess the role of the epithelium in regulating airway tone using the intact guinea pig trachea (J. Appl. Physiol. 64: 466–471, 1988). This method allows us to study the response of the airway when its inner epithelial surface or its outer serosal surface is stimulated independently. Using this system we evaluated how the presence of intact epithelium can affect pharmacological responsiveness. We first examined responses of tracheae with intact epithelium to histamine, acetylcholine, and hypertonic KCl when stimulated from the epithelial or serosal side. We then examined the effect of epithelial denudation on the responses to these agonists. With an intact epithelium, stimulation of the inner epithelial side always caused significantly smaller changes in diameter than stimulation of the outer serosal side. After mechanical denudation of the epithelium, these differences were almost completely abolished. In the absence of intact epithelium, the trachea was 35-fold more sensitive to histamine and 115-fold more sensitive to acetylcholine when these agents were applied to the inner epithelial side. In addition, the presence of an intact epithelium almost completely inhibited any response to epithelial side challenge with hypertonic KCl. These results indicate that the airway epithelial layer has a potent protective role in airway responses to luminal side stimuli, leading us to speculate that changes in airway reactivity measured in various conditions including asthma may result in part from changes in epithelial function.
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Son, Joung A., Joung A. Son, Taizo Hogetsu, Joung A. Son, Taizo Hogetsu, and Yil-Sung Moon. "The process of epithelial cell death in Pinus thunbergii caused by the pine wood nematode, Bursaphelenchus xylophilus." Nematology 16, no. 6 (2014): 663–68. http://dx.doi.org/10.1163/15685411-00002795.
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This study describes a new technique to investigate how the pine wood nematode (PWN), Bursaphelenchus xylophilus, kills pine epithelial cells. After inoculating PWN into 20-cm-long Pinus thunbergii stem cuttings and incubating for 1, 3 or 7 days, the cuttings were split into 2.5 cm segments. The segments were tangentially cut so that the epithelia of several cortical resin canals were exposed, and these were stained with Evans Blue for the detection of dead epithelial cells. While almost no dead epithelial cells were found in the cortical resin canals of non-PWN-inoculated control cuttings up to day 7 of the experiment, dead epithelial cells were distributed sparsely in the epithelium of cortical resin canals throughout pine cuttings inoculated with PWN 1, 3 and 7 days after inoculation. The sparse and sporadic distribution of dead pine cells in the epithelium suggested that individual PWN attacked one epithelial cell at a time with its stylet and migrated between attacks.
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Farman, N., C. R. Talbot, R. Boucher, M. Fay, C. Canessa, B. Rossier, and J. P. Bonvalet. "Noncoordinated expression of alpha-, beta-, and gamma-subunit mRNAs of epithelial Na+ channel along rat respiratory tract." American Journal of Physiology-Cell Physiology 272, no. 1 (January 1, 1997): C131—C141. http://dx.doi.org/10.1152/ajpcell.1997.272.1.c131.
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Na+ reabsorption from the epithelial surface of the respiratory tract plays a fundamental role in respiratory physiology. As in the epithelia of the renal collecting tubule and distal colon, Na+ enters across the luminal surface of respiratory epithelial cells via a recently cloned amiloride-sensitive multisubunit (alpha, beta, gamma) epithelial Na+ channel. We have examined the cellular expression at the mRNA level of the alpha-, beta-, and gamma-subunits of rat epithelial Na+ channel (rENaC) in the rat lung and upper airway epithelial cells using in situ hybridization. A large prevalence of alpha- and gamma-rENaC subunit expression (over beta) was found in tracheal epithelium, in a subpopulation of alveolar cells, presumably type II pneumocytes, and in nasal and tracheal gland acini. In contrast, equivalent levels of expression of all three subunits were detected in bronchiolar epithelium and in rat nasal gland ducts. This diversity of expression may reflect cell-specific functions of the amiloride-sensitive Na+ channel along the respiratory tract.
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Hama, Seiji, Kazunori Arita, Takashi Nishisaka, Toshiyuki Fukuhara, Atsushi Tominaga, Kazuhiko Sugiyama, Hiroyuki Yoshioka, et al. "Changes in the epithelium of Rathke cleft cyst associated with inflammation." Journal of Neurosurgery 96, no. 2 (February 2002): 209–16. http://dx.doi.org/10.3171/jns.2002.96.2.0209.
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Object. Rathke cleft cysts (RCCs) are composed of tall, well-differentiated, ciliated columnar epithelia. Their structures are altered by hyperplasia or squamous metaplasia, but their cause remains unknown. Methods. The authors studied pathological findings and anterior pituitary function in 20 patients harboring RCCs. They classified RCC epithelium as either single (a single ciliated columnar cell lining or a flattened cuboidal cell lining) or stratified (a stratified ciliated columnar cell lining, basal cell hyperplasia, columnar cell hyperplasia, or squamous metaplasia). Inflammation was classified as acute, subacute, chronic, or end stage. The epithelial cell lining was observed in 13 specimens obtained during surgery (six specimens contained single and seven contained stratified epithelia). Inflammation had penetrated the cyst epithelium or subjacent stroma in 10 patients, and the stage of inflammation correlated well with the type of epithelia group: early stages of inflammation in the single epithelium group and chronic or end-stage inflammation in the stratified epithelia (p = 0.0027). The adenohypophysis was identified in 21 surgical specimens. Postoperatively, growth hormone (p = 0.019), cortisol (p = 0.027), and thyroid-stimulating hormone (p = 0.039) responses significantly worsened as the inflammation progressed. The presence of diabetes insipidus correlated well with advanced stages of neurohypophysitis (p = 0.025). Conclusions. Epithelial stratification in the RCC is caused by inflammation that may extend into the adjacent adenohypophysis or neurohypophysis and overwhelm the hypophysis, resulting in panhypopituitarism. Transsphenoidal excision may represent the best choice for treatment, at least for cases of RCC in which there is partial impairment of hypophysial function.
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Nakajima, Tadaaki, Yuki Tanimoto, Masami Tanaka, Pierre Chambon, Hajime Watanabe, Taisen Iguchi, and Tomomi Sato. "Neonatal Estrogen Receptor β Is Important in the Permanent Inhibition of Epithelial Cell Proliferation in the Mouse Uterus." Endocrinology 156, no. 9 (May 28, 2015): 3317–28. http://dx.doi.org/10.1210/en.2015-1012.
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Estrogen receptor α (ERα) plays a pivotal role in the mouse uterine and vaginal epithelial cell proliferation stimulated by estrogen, whereas ERβ inhibits cell proliferation. ERβ mRNA is expressed in neonatal uteri and vaginae; however, its functions in neonatal tissues have not been ascertained. In this study, we investigated the ontogenic mRNA expression and localization of ERβ, and its roles in cell proliferation in neonatal uteri and vaginae of ERβ knockout (βERKO) mice. ERβ mRNA and protein were abundant in the uterine and vaginal epithelia of 2-day-old mice and decreased with age. In uterine and vaginal epithelia of 2-day-old βERKO mice, cell proliferation was greater than that in wild-type animals and in uterine epithelia of 90- and 365-day-old βERKO mice. In addition, p27 protein, known as a cyclin-dependent kinase inhibitor, was decreased in the uteri of 90- and 365-day-old βERKO mice. Inhibition of neonatal ERs by ICI 182780 (an ER antagonist) treatment stimulated cell proliferation and decreased p27 protein in the uterine luminal epithelium of 90-day-old mice but not in the vaginal epithelium. These results suggest that neonatal ERβ is important in the persistent inhibition of epithelial cell proliferation with accumulation of p27 protein in the mouse uterus. Thus, suppression of ERβ function in the uterine epithelium during the neonatal period may be responsible for a risk for proliferative disease in adults.
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Delplanque, A., C. Coraux, R. Tirouvanziam, I. Khazaal, E. Puchelle, P. Ambros, D. Gaillard, and B. Peault. "Epithelial stem cell-mediated development of the human respiratory mucosa in SCID mice." Journal of Cell Science 113, no. 5 (March 1, 2000): 767–78. http://dx.doi.org/10.1242/jcs.113.5.767.
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We have developed an in vivo assay for progenitor cells of the human tracheobronchial epithelium relying on the transplantation of human prenatal respiratory tissues into severe combined immunodeficiency mice. Engrafted embryonic or fetal open tracheobronchial rudiments are rapidly closed at each end by a neoformed membrane that we named the operculum. After 2–4 weeks, differentiated human respiratory epithelium covers both the native airway matrix and the new operculum. Human epithelial cells dissociated from either emerging embryonic lung primordia or mature xenografts were seeded in host human airway grafts, of which native epithelium had been eliminated by several cycles of freezing and thawing. All grafts seeded with donor epithelial cells and implanted back into SCID mice recovered a surface mucociliary epithelium expressing expected markers and secreting mucus. Spontaneous epithelium regrowth was never observed in control unseeded, denuded grafts. In some experiments, donor epithelial cells and host denuded airway were sex-mismatched and the donor origin of newly formed epithelial structures was confirmed by sex chromosome detection. After two rounds of seeding and reimplantation, a normal epithelium was observed to line the 3rd generation operculum. These observations substantiate a functional assay for human candidate airway epithelium stem cells.
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Gonzalez-Escobedo, Geoffrey, and John S. Gunn. "Gallbladder Epithelium as a Niche for Chronic Salmonella Carriage." Infection and Immunity 81, no. 8 (June 3, 2013): 2920–30. http://dx.doi.org/10.1128/iai.00258-13.
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ABSTRACTAlthough typhoid fever has been intensively studied, chronic typhoid carriage still represents a problem for the transmission and persistence of the disease in areas of endemicity. This chronic state is highly associated with the presence of gallstones in the gallbladder of infected carriers upon whichSalmonellacan form robust biofilms. However, we hypothesize that in addition to gallstones, the gallbladder epithelium aids in the establishment/maintenance of chronic carriage. In this work, we present evidence of the role of the gallbladder epithelium in chronic carriage by a mechanism involving invasion, intracellular persistence, and biofilm formation.Salmonellawas able to adhere to and invade polarized gallbladder epithelial cells apically in the absence and presence of bile in aSalmonellapathogenicity island 1 (SPI-1)-dependent manner. Intracellular replication ofSalmonellawas also evident at 12 and 24 h postinvasion. A flowthrough system revealed thatSalmonellais able to adhere to and form extensive bacterial foci on gallbladder epithelial cells as early as 12 h postinoculation.In vivoexperiments using a chronic mouse model of typhoid carriage showed invasion and damage of the gallbladder epithelium and lamina propria up to 2 months afterSalmonellainfection, with an abundant presence of macrophages, a relative absence of neutrophils, and extrusion of infected epithelial cells. Additionally, microcolonies ofSalmonellacells were evident on the surface of the mouse gallbladder epithelia up to 21 days postinfection. These data reveal a second potential mechanism, intracellular persistence and/or bacterial aggregation in/on the gallbladder epithelium with luminal cell extrusion, forSalmonellamaintenance in the gallbladder.
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Juodziukyniene, Nomeda, and Albina Aniuliene. "Histomorphometric study of the canine prostate during ageing and in cases of benign prostate hyperplasia." Journal of Veterinary Research 60, no. 1 (March 1, 2016): 91–97. http://dx.doi.org/10.1515/jvetres-2016-0013.
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AbstractIntroduction: The aim of the study was to examine the percentage volume of epithelium, acini, and interstitial collagen in the nonhyperplastic canine prostate and in cases of epithelial and epithelial cystic hyperplasia. Material and Methods: A histomorphometric study of 39 prostates was performed using computer image analysis. Results: The highest percentage volume of epithelium was found in cases of epithelial hyperplasia (47.8 %) and epithelial cystic hyperplasia was the correlate for acini (48.97 %). Epithelium decreased with dogs’ age (P < 0.01), whereas acini increased (P < 0.01). Interstitial collagen varied only insignificantly across age groups, but collagen was higher (12.1 %) in the nonhyperplastic prostates. With age cystic formation progressed in the canine prostate, the percentage volume of epithelium decreased and that of acini increased, but this same parameter in prostatic collagen did not change distinctly. The epithelium percentage volume increased in cases of epithelial hyperplasia but the cystic variant caused an increase in acinar volume. Conclusion: As dogs age, cystic formation progresses in the prostate, therefore the volume of epithelium decreases and that of acini increases. The volume of prostatic collagen did not change distinctly with age, and was higher in normal prostates than in both epithelial and epithelial cystic hyperplastic glands.
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Brisken, Cathrin, Anna Heineman, Tony Chavarria, Brian Elenbaas, Jian Tan, Sudhansu K. Dey, Jill A. McMahon, Andrew P. McMahon, and Robert A. Weinberg. "Essential function of Wnt-4 in mammary gland development downstream of progesterone signaling." Genes & Development 14, no. 6 (March 15, 2000): 650–54. http://dx.doi.org/10.1101/gad.14.6.650.
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Female reproductive hormones control mammary gland morphogenesis. In the absence of the progesterone receptor (PR) from the mammary epithelium, ductal side-branching fails to occur. We can overcome this defect by ectopic expression of the protooncogene Wnt-1. Transplantation of mammary epithelia fromWnt-4−/− mice shows that Wnt-4 has an essential role in side-branching early in pregnancy. PR andWnt-4 mRNAs colocalize to the luminal compartment of the ductal epithelium. Progesterone induces Wnt-4 in mammary epithelial cells and is required for increased Wnt-4 expression during pregnancy. Thus, Wnt signaling is essential in mediating progesterone function during mammary gland morphogenesis.
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Troyanovsky, S. M., V. I. Guelstein, T. A. Tchipysheva, V. A. Krutovskikh, and G. A. Bannikov. "Patterns of expression of keratin 17 in human epithelia: dependency on cell position." Journal of Cell Science 93, no. 3 (July 1, 1989): 419–26. http://dx.doi.org/10.1242/jcs.93.3.419.
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By immunomorphology, using keratin 17-specific monoclonal antibody, it has been shown that this keratin is expressed only in the basal cells of a group of complex epithelia: glandular epithelium with myoepithelial component, transitional and pseudostratified epithelia. Immunolocalization of keratin 17 provides evidence that the expression of this keratin strongly depends on the cell position within epithelial structures. The topographical character of the keratin expression suggests that these proteins may be implicated in the generation of spatial organization of epithelial tissues.
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Bassnett, S., J. R. Kuszak, L. Reinisch, H. G. Brown, and D. C. Beebe. "Intercellular communication between epithelial and fiber cells of the eye lens." Journal of Cell Science 107, no. 4 (April 1, 1994): 799–811. http://dx.doi.org/10.1242/jcs.107.4.799.
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Results of electrical, dye-coupling and morphological studies have previously suggested that gap junctions mediate communication between the anterior epithelium of the lens and the underlying lens fiber cells. This connection is believed to permit ‘metabolic cooperation’ between these dissimilar cell types and may be of particular importance to the fiber cells, which are thought incapable of autonomous ionic homeostasis. We reinvestigated the nature of the connection between epithelial and fiber cells of the embryonic chicken lens using fluorescence confocal microscopy and freeze-fracture analysis. In contrast to earlier studies, our data provided no support for gap-junction-mediated transport from the lens epithelium to the fibers. Fluorescent dyes loaded biochemically into the lens epithelium were retained there for more than one hour. There was a decrease in epithelial fluorescence over this period, but this was not accompanied by an increase in fiber cell fluorescence. Diffusional modeling suggested that these data were inconsistent with the presence of extensive epithelium-fiber cell coupling, even if the observed decrease in epithelial fluorescence was attributed exclusively to the diffusion of dye into the fiber mass via gap junctions. Furthermore, the rate of loss of fluorescence from isolated epithelia was indistinguishable from that measured in whole lenses, suggesting that decreased epithelial fluorescence resulted from photobleaching and leakage of dye rather than diffusion, via gap junctions, into the fibers. Analysis of freeze-fracture replicas of plasma membranes at the epithelial-fiber cell interface failed to reveal evidence of gap-junction plaques, although evidence of endocytosis was abundant. These studies were done under conditions where the location of the fracture plane was unambiguous and where gap junctions could be observed in the lateral membranes of neighboring epithelial and fiber cells. Paradoxically, tracer molecules injected into the fiber mass were able to pass into the epithelium via a pathway that was not blocked by incubation at 4 degrees C or by treatment with octanol and which excluded large (approximately 10 kDa) molecular mass tracers. Together with previous measurements of electrical coupling between fiber cells and epithelial cells, these data indicate the presence of a low-resistance pathway connecting these cell types that is not mediated by classical gap junctions.
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Klein-Szanto, Andres J. P., Hitoshi Ura, and James Resau. "Formaldehyde-Induced Lesions of Xenotransplanted Human Nasal Respiratory Epithelium." Toxicologic Pathology 17, no. 1_part_1 (January 1989): 33–37. http://dx.doi.org/10.1177/01926233890171p105.
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Cells from the nasal respiratory epithelium were obtained at autopsy from young adults, amplified in primary cultures, and inoculated into de-epithelialized rat tracheas. These tracheas were sealed and transplanted subcutaneously into irradiated nude mice. Four weeks after this xenotransplantation procedure, when the tracheal lumina were covered by normal respiratory epithelium, the transplants were exposed to slow releasing silastic devices containing 0,0.5 or 1 mg paraformaldehyde. Histological examination supplemented with autoradiographies revealed that the aldehyde produced both involutional changes such as erosion and atrophic epithelium and proliferative reactions such as hyperplastic-metaplastic lesions. These epithelial changes were characterized by a higher labeling index that in some focal areas reached values 10 to 20 times higher than normal. These effects were noted 2 weeks after exposure with FMD and in an attenuated form could also be seen at 8 weeks. This response pattern is very similar to that of the xenotransplanted human tracheobronchial epithelium and also of the rat nasal and tracheobronchial epithelia, in which formaldehyde proved to be an effective carcinogen.