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Journal articles on the topic 'Epithelial cells'
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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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Sun, Tung-Tien. "Altered phenotype of cultured urothelial and other stratified epithelial cells: implications for wound healing." American Journal of Physiology-Renal Physiology 291, no. 1 (July 2006): F9—F21. http://dx.doi.org/10.1152/ajprenal.00035.2006.
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The differentiation of cultured stratified epithelial cells can deviate significantly from that of normal epithelium, leading to suggestions that cultured cells undergo abnormal differentiation, or a truncated differentiation. Thus cultured epidermal and corneal epithelial cells stop synthesizing their tissue-specific keratin pair K1/K10 and K3/K12, respectively. The replacement of these keratins in the suprabasal compartment by K6/K16 keratins that are made by all stratified squamous epithelia during hyperplasia rules out a truncated differentiation. Importantly, the keratin pattern of in vivo corneal epithelium undergoing wound repair mimics that of cultured rabbit corneal epithelial cells. Although cultured urothelial cells continue to synthesize uroplakins, which normally form two-dimensional crystalline urothelial plaques covering almost the entire apical urothelial surface, these proteins do not assemble into crystals in cultured cells. Cultured epithelial cells can, however, rapidly regain normal differentiation on the removal of mitogenic stimuli, the use of a suitable extracellular matrix, or the transplantation of the cells to an in vivo, nonmitogenic environment. These data suggest that cultured epithelial cells adopt altered differentiation patterns mimicking in vivo regenerating or hyperplastic epithelia. Blocking the synthesis of tissue-specific differentiation products, such as the K1 and K10 keratins designed to form extensive disulfide cross-links in cornified cells, or the assembly of uroplakin plaques allows epithelial cells to better migrate and proliferate, activities that are of overriding importance during wound repair. Cultured urothelial and other stratified epithelial cells provide excellent models for studying the regulation of the synthesis and assembly of differentiation products, a key cellular process during epithelial wound repair.
3
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.
4
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.
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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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Ohmoto, Makoto, Shugo Nakamura, Hong Wang, Peihua Jiang, Junji Hirota, and Ichiro Matsumoto. "Maintenance and turnover of Sox2+ adult stem cells in the gustatory epithelium." PLOS ONE 17, no. 9 (September 2, 2022): e0267683. http://dx.doi.org/10.1371/journal.pone.0267683.
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Continuous turnover of taste bud cells in the oral cavity underlies the homeostasis of taste tissues. Previous studies have demonstrated that Sox2+ stem cells give rise to all types of epithelial cells including taste bud cells and non-gustatory epithelial cells in the oral epithelium, and Sox2 is required for generating taste bud cells. Here, we show the dynamism of single stem cells through multicolor lineage tracing analyses in Sox2-CreERT2; Rosa26-Confetti mice. In the non-gustatory epithelium, unicolored areas populated by a cluster of cells expressing the same fluorescent protein grew over time, while epithelial cells were randomly labeled with multiple fluorescent proteins by short-term tracing. Similar phenomena were observed in gustatory epithelia. These results suggest that the Sox2+ stem cell population is maintained by balancing the increase of certain stem cells with the reduction of the others. In the gustatory epithelia, many single taste buds contained cells labeled with different fluorescent proteins, indicating that a single taste bud is composed of cells derived from multiple Sox2+ stem cells. Our results reveal the characteristics of Sox2+ stem cells underlying the turnover of taste bud cells and the homeostasis of taste tissues.
7
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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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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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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Yu, Qian, Liang-Chun Wang, Sofia Di Benigno, Daniel C. Stein, and Wenxia Song. "Gonococcal invasion into epithelial cells depends on both cell polarity and ezrin." PLOS Pathogens 17, no. 12 (December 1, 2021): e1009592. http://dx.doi.org/10.1371/journal.ppat.1009592.
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Neisseria gonorrhoeae (GC) establishes infection in women from the cervix, lined with heterogeneous epithelial cells from non-polarized stratified at the ectocervix to polarized columnar at the endocervix. We have previously shown that GC differentially colonize and transmigrate across the ecto and endocervical epithelia. However, whether and how GC invade into heterogeneous cervical epithelial cells is unknown. This study examined GC entry of epithelial cells with various properties, using human cervical tissue explant and non-polarized/polarized epithelial cell line models. While adhering to non-polarized and polarized epithelial cells at similar levels, GC invaded into non-polarized more efficiently than polarized epithelial cells. The enhanced GC invasion in non-polarized epithelial cells was associated with increased ezrin phosphorylation, F-actin and ezrin recruitment to GC adherent sites, and the elongation of GC-associated microvilli. Inhibition of ezrin phosphorylation inhibited F-actin and ezrin recruitment and microvilli elongation, leading to a reduction in GC invasion. The reduced GC invasion in polarized epithelial cells was associated with non-muscle myosin II-mediated F-actin disassembly and microvilli denudation at GC adherence sites. Surprisingly, intraepithelial GC were only detected inside epithelial cells shedding from the cervix by immunofluorescence microscopy, but not significantly in the ectocervical and the endocervical regions. We observed similar ezrin and F-actin recruitment in exfoliated cervical epithelial cells but not in those that remained in the ectocervical epithelium, as the luminal layer of ectocervical epithelial cells expressed ten-fold lower levels of ezrin than those beneath. However, GC inoculation induced F-actin reduction and myosin recruitment in the endocervix, similar to what was seen in polarized epithelial cells. Collectively, our results suggest that while GC invade non-polarized epithelial cells through ezrin-driven microvilli elongation, the apical polarization of ezrin and F-actin inhibits GC entry into polarized epithelial cells.
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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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Varsano, S., S. C. Lazarus, W. M. Gold, and J. A. Nadel. "Selective adhesion of mast cells to tracheal epithelial cells in vitro." Journal of Immunology 140, no. 7 (April 1, 1988): 2184–92. http://dx.doi.org/10.4049/jimmunol.140.7.2184.
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Abstract In allergic and nonallergic lung diseases, if intraluminal mast cells adhere to airway epithelium, inflammatory mediators released from activated mast cells may reach high local concentrations and thus greatly affect airway function. To determine whether mast cells adhere to airway epithelial cells, radiolabeled or unlabeled dog mastocytoma cells were incubated with cultured dog tracheal epithelial cells, with extracellular matrix substrates, and with cryostat-cut sections of dog trachea. Mast cells adhered well to cultured epithelial cells (35 +/- 13% adhesion, mean +/- 1 SD, n = 23) but adhered poorly to types I and IV collagen or to fibronectin (less than 7.5% mean adhesion in all cases). Similarly, in tracheal tissue sections, mast cells adhered preferentially to epithelial cells in surface epithelium or in submucosal glands but not to basal membrane or connective tissue. Adhesion to cultured epithelial cells was a characteristics of a subpopulation of mast cells, could persist for more than 48 h, did not require energy or the presence of divalent cations, and was not mediated by a known family of leukocyte-associated adhesion glycoproteins. Adhesion was completely abolished by pretreatment of mast cells with pronase E or proteinase K but not with trypsin (up to 10 micrograms/ml at 37 degrees C for 20 min each). In contrast, pretreatment of cultured epithelial cells with any of these proteinases had no effect on adhesion. It is concluded that dog mastocytoma mast cells adhere to dog tracheal epithelial cells and do so selectively. It is suggested that mast cell adhesion to airway epithelium may play a role in the effectiveness of mast cell-epithelial cell interactions, and thus, in certain lung diseases, airway function may be affected by intraluminal mast cells more than is currently appreciated.
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Macpherson, A. J., T. P. Mayall, K. A. Chester, A. Abbasi, I. Forgacs, A. D. Malcolm, and T. J. Peters. "Mitochondrial gene expression in the human gastrointestinal tract." Journal of Cell Science 102, no. 2 (June 1, 1992): 307–14. http://dx.doi.org/10.1242/jcs.102.2.307.
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In the human gastrointestinal epithelium, in situ hybridisation demonstrates that 12 S and 16 S mitochondrial ribosomal RNAs show maximal steady-state levels on the surface epithelial cells of the normal small intestine and colon. The mitochondrial mRNAs, cytochrome b and NADH dehydrogenase (IV) have a uniform distribution throughout the crypt and surface (villus) epithelial cells of the small intestine and colon. Histochemical stains for the activity of the mitochondrial respiratory chain enzymes succinate dehydrogenase and cytochrome oxidase also show almost uniform activities throughout the crypt-surface epithelial cell axis in the small and large intestines. In sections of normal human oesophagus the levels of mitochondrial ribosomal RNAs, mitochondrial mRNAs and the activities of mitochondrial respiratory chain enzymes are maximal over the basal cells of the stratified squamous epithelium. These results show a relative increase in mitochondrial ribosomal RNA expression compared with mitochondrial mRNAs in surface cells of simple intestinal epithelia.
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Wu, John H., Barry J. Billings, and Daniel F. Balkovetz. "Hepatocyte Growth Factor Alters Renal Epithelial Cell Susceptibility to Uropathogenic Escherichia coli." Journal of the American Society of Nephrology 12, no. 12 (December 2001): 2543–53. http://dx.doi.org/10.1681/asn.v12122543.
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ABSTRACT. The urinary tract is frequently the source of Escherichia coli bacteremia. Bacteria from the urinary tract must cross an epithelial layer to enter the bloodstream. Hepatocyte growth factor (HGF) alters the polarity of Madin-Darby canine kidney (MDCK) epithelial cells. The role of cell polarity in determining renal epithelial resistance to Escherichia coli invasion is not well known. A model of polarized and HGF-treated MDCK epithelial cells grown on filters was used to study the role of epithelial cell polarity during the interaction of nonvirulent (XL1-Blue) and uropathogenic (J96) strains of Escherichia coli with renal epithelium. Basolateral exposure of MDCK cells to J96, but not XL1-Blue, resulted in loss of transepithelial resistance (TER), which was due to epithelial cytotoxicity and not degradation of epithelial junctional proteins by bacterial proteases. Apical exposure to both J96 and XL1-Blue did not alter TER. Pretreatment of polarized MDCK cell monolayers with HGF renders the cells sensitive to loss of TER and cytotoxicity by apical exposure to J96. Analysis by confocal microscopy demonstrated that HGF treatment of MDCK cell monolayers also greatly enhances adherence of J96 to the apical surface of the cell monolayer. These data demonstrate that the basolateral surface of polarized epithelia is more susceptible to J96 cytotoxicity. The data also support the hypothesis that processes that alter epithelial cell polarity increase sensitivity of epithelia to bacterial injury and adherence from the apical compartment.
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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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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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Verburg, Melissa, Ingrid B. Renes, Helen P. Meijer, Jan A. J. M. Taminiau, Hans A. Büller, Alexandra W. C. Einerhand, and Jan Dekker. "Selective sparing of goblet cells and Paneth cells in the intestine of methotrexate-treated rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 5 (November 1, 2000): G1037—G1047. http://dx.doi.org/10.1152/ajpgi.2000.279.5.g1037.
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Proliferation, differentiation, and cell death were studied in small intestinal and colonic epithelia of rats after treatment with methotrexate. Days 1–2 after treatment were characterized by decreased proliferation, increased apoptosis, and decreased numbers and depths of small intestinal crypts in a proximal-to-distal decreasing gradient along the small intestine. The remaining crypt epithelium appeared flattened, except for Paneth cells, in which lysozyme protein and mRNA expression was increased. Regeneration through increased proliferation during days 3–4 coincided with villus atrophy, showing decreased numbers of villus enterocytes and decreased expression of the enterocyte-specific genes sucrase-isomaltase and carbamoyl phosphate synthase I. Remarkably, goblet cells were spared at villus tips and remained functional, displaying Muc2 and trefoil factor 3 expression. On days 8–10, all parameters had returned to normal in the whole small intestine. No methotrexate-induced changes were seen in epithelial morphology, proliferation, apoptosis, Muc2, and TFF3 immunostaining in the colon. The observed small intestinal sparing of Paneth cells and goblet cells following exposure to methotrexate is likely to contribute to epithelial defense during increased vulnerability of the intestinal epithelium.
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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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Khan, Ayyad Z., Tor P. Utheim, Catherine J. Jackson, Sjur Reppe, Torstein Lyberg, and Jon R. Eidet. "Nucleus Morphometry in Cultured Epithelial Cells Correlates with Phenotype." Microscopy and Microanalysis 22, no. 3 (June 2016): 612–20. http://dx.doi.org/10.1017/s1431927616000830.
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AbstractPhenotype of cultured ocular epithelial transplants has been shown to affect clinical success rates following transplantation to the cornea. The purpose of this study was to evaluate the relationship between cell nucleus morphometry and phenotype in three types of cultured epithelial cells. This study provides knowledge for the development of a non-invasive method of determining the phenotype of cultured epithelium before transplantation. Cultured human conjunctival epithelial cells (HCjE), human epidermal keratinocytes (HEK), and human retinal pigment epithelial cells (HRPE) were analyzed by quantitative immunofluorescence. Assessments of nucleus morphometry and nucleus-to-cytoplasm ratio (N/C ratio) were performed using ImageJ. Spearman’s correlation coefficient was employed for statistical analysis. Levels of the proliferation marker PCNA in HCjE, HEK, and HRPE correlated positively with nuclear area. Nuclear area correlated significantly with levels of the undifferentiated cell marker ABCG2 in HCjE. Bmi1 levels, but not p63α levels, correlated significantly with nuclear area in HEK. The N/C ratio did not correlate significantly with any of the immunomarkers in HCjE (ABCG2, CK7, and PCNA) and HRPE (PCNA). In HEK, however, the N/C ratio was negatively correlated with levels of the undifferentiated cell marker CK14 and positively correlated with Bmi1 expression. The size of the nuclear area correlated positively with proliferation markers in all three epithelia. Morphometric indicators of phenotype in cultured epithelia can be identified using ImageJ. Conversely, the N/C ratio did not show a uniform relationship with phenotype in HCjE, HEK, or HRPE. N/C ratio therefore, may not be a useful morphometric marker for in vitro assessment of phenotype in these three epithelia.
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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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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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Cramer, E. B., L. C. Milks, M. J. Brontoli, G. K. Ojakian, S. D. Wright, and H. J. Showell. "Effect of human serum and some of its components on neutrophil adherence and migration across an epithelium." Journal of Cell Biology 102, no. 5 (May 1, 1986): 1868–77. http://dx.doi.org/10.1083/jcb.102.5.1868.
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The effect of human serum and some of its components on the process of transepithelial migration of human neutrophils was investigated in an in vitro system. 10% autologous serum caused an increase in neutrophil adherence to and migration across canine kidney epithelial cells. This increase in neutrophil binding also occurred if the epithelium but not the neutrophils had been preincubated with serum. The binding was lost if the serum was either preabsorbed over the kidney epithelium before use or heat inactivated. Indirect immunofluorescence studies indicated that IgG, IgM, and a component of C3 bound to the epithelial surface, whereas IgA, IgE, or C5a were not detectable. The majority of epithelial cells were immunofluorescent, however epithelial cells with varying degrees of reactivity were also apparent and approximately 5% of the epithelial cells did not bind IgG, IgM, and C3. When epithelia were simultaneously tested for the presence of either IgG, IgM, or C3, and bound neutrophils the few epithelial cells which did not bind IgG or IgM also did not bind C3 or neutrophils. Studies with monoclonal antibodies against Fc and C3 receptors indicate that neutrophil adherence to the epithelial surface was mediated predominately by the receptors for C3b and C3bi. In response to a chemotactic gradient, bound neutrophils were able to detach and migrate across the epithelium. A separate heat-stable factor(s) in serum was able to increase neutrophil migration across the epithelial monolayer. This factor acted independently of the factors which caused the increase in neutrophil binding as the increase in neutrophil migration also occurred under conditions (preabsorption over the kidney epithelium or heat inactivation) that prevented the increase in neutrophil binding. The increase in neutrophil migration may be caused by the permeability-increasing properties of this factor as both serum and heat-inactivated serum lowered the transepithelial electrical resistance an average of 38 and 35%, respectively, in 40 min. Upon removal of serum or heat-inactivated serum, the resistance returned 100 and 81%, respectively, in 5 h.
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Lochter, André. "Plasticity of mammary epithelia during normal development and neoplastic progression." Biochemistry and Cell Biology 76, no. 6 (December 1, 1998): 997–1008. http://dx.doi.org/10.1139/o99-010.
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The functional unit of the mammary gland is the epithelium. It consists of luminal epithelial cells and myoepithelial cells that are generated from self-renewing stem and progenitor cells. The latter two cell types are scattered throughout the mammary epithelium and are concentrated in specialized structures, the end buds. In transplantation studies the pluripotency of mammary stem cells has been confirmed by demonstrating that they can regenerate a complete mammary gland. The ability of mammary epithelial cells to produce an elaborate ductal system during puberty and to differentiate into milk-producing alveoli during pregnancy is not only influenced by their genetic make-up, but is also governed by local molecular signals. Recent studies suggest that the transdifferentiation of epithelial cells into tumor cells is under microenvironmental control, despite the prominence of genetic mutations in breast cancer. Consequently, disturbances of tissue homeostasis can alter mammary gland development or result in preneoplastic and neoplastic pathologies. The plasticity of mammary epithelia is not limited to the entry of cells into differentiation and transdifferentiation pathways, but extends to their ability to regain facets of their preceding stage of functionality. Deciphering the molecular cues that determine cell plasticity is prerequisite for establishing a unifying concept of mammary gland development and breast tumor progression.Key words: branching morphogenesis, lactogenic differentiation, stem cells, epithelial-to-mesenchymal transition, cancer.
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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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Lin, Zhen, Kenneth Swan, Xin Zhang, Subing Cao, Zoe Brett, Stacy Drury, Michael J. Strong, et al. "Secreted Oral Epithelial Cell Membrane Vesicles Induce Epstein-Barr Virus Reactivation in Latently Infected B Cells." Journal of Virology 90, no. 7 (January 13, 2016): 3469–79. http://dx.doi.org/10.1128/jvi.02830-15.
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ABSTRACTIn the oral epithelium, peripheral stores of Epstein-Barr virus (EBV) are transmitted from infiltrating B cells to epithelial cells. Once the virus is transmitted to epithelial cells, the highly permissive nature of this cell type for lytic replication allows virus amplification and exchange to other hosts. Since the initial transfer of EBV from B cells to epithelial cells requires transitioning of the B-cell to a state that induces virus reactivation, we hypothesized that there might be epithelium-specific signals that allow the infiltrating B cells to sense the appropriate environment to initiate reactivation and begin this exchange process. We previously found that the epithelium-specific miR-200 family of microRNAs promotes EBV lytic replication. Here we show that there are high levels of miR-200 family members in oral and tonsillar epithelia and in saliva. Analysis of cultured oral epithelial cells (OKF6) showed that they actively secrete membrane vesicles (exosomes) that are enriched with miR-200 family members. Coculturing of EBV-positive B cells with OKF6 cells induced viral reactivation. Further, treatment of EBV-positive B cells with OKF6 cell-derived membrane vesicles promoted reactivation. Using a cell system that does not naturally express miR-200 family members, we found that enforced expression of a miR-200 family member produced membrane vesicles that were able to induce the lytic cascade in EBV-positive B cells. We propose that membrane vesicles secreted by oral and tonsillar epithelial cells may serve as a tissue-specific environmental cue that initiates reactivation in B cells, promoting the transfer of virus from peripheral B-cell stores to the oral epithelium to facilitate virus amplification and exchange to other hosts.IMPORTANCEEpstein-Barr virus (EBV) is an important human pathogen that is causally associated with several lymphomas and carcinomas. The switch from latency to the lytic cycle is critical for successful host infection and for EBV pathogenesis. Although the EBV lytic cycle can be triggered by certain agentsin vitro, the mechanisms that signal reactivationin vivoare poorly understood. We previously reported that endogenously expressed miR-200 family members likely play a role in facilitating the lytic tendencies of EBV in epithelial cells. Here we show that membrane vesicles secreted from oral epithelial cells contain miR-200 family members and that they can be transmitted to proximal EBV-positive B cells, where they trigger reactivation. We propose that this intercellular communication pathway may serve as a sensor mechanism for infiltrating B cells to recognize an appropriate environment to initiate reactivation, thereby allowing the exchange of virus to the oral epithelium.
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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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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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Hamilton, Nick J. I., Dani Do Hyang Lee, Kate H. C. Gowers, Colin R. Butler, Elizabeth F. Maughan, Benjamin Jevans, Jessica C. Orr, et al. "Bioengineered airway epithelial grafts with mucociliary function based on collagen IV- and laminin-containing extracellular matrix scaffolds." European Respiratory Journal 55, no. 6 (May 22, 2020): 1901200. http://dx.doi.org/10.1183/13993003.01200-2019.
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Current methods to replace damaged upper airway epithelium with exogenous cells are limited. Existing strategies use grafts that lack mucociliary function, leading to infection and the retention of secretions and keratin debris. Strategies that regenerate airway epithelium with mucociliary function are clearly desirable and would enable new treatments for complex airway disease.Here, we investigated the influence of the extracellular matrix (ECM) on airway epithelial cell adherence, proliferation and mucociliary function in the context of bioengineered mucosal grafts. In vitro, primary human bronchial epithelial cells (HBECs) adhered most readily to collagen IV. Biological, biomimetic and synthetic scaffolds were compared in terms of their ECM protein content and airway epithelial cell adherence.Collagen IV and laminin were preserved on the surface of decellularised dermis and epithelial cell attachment to decellularised dermis was greater than to the biomimetic or synthetic alternatives tested. Blocking epithelial integrin α2 led to decreased adherence to collagen IV and to decellularised dermis scaffolds. At air–liquid interface (ALI), bronchial epithelial cells cultured on decellularised dermis scaffolds formed a differentiated respiratory epithelium with mucociliary function. Using in vivo chick chorioallantoic membrane (CAM), rabbit airway and immunocompromised mouse models, we showed short-term preservation of the cell layer following transplantation.Our results demonstrate the feasibility of generating HBEC grafts on clinically applicable decellularised dermis scaffolds and identify matrix proteins and integrins important for this process. The long-term survivability of pre-differentiated epithelia and the relative merits of this approach against transplanting basal cells should be assessed further in pre-clinical airway transplantation models.
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Laitinen, L. "Epithelial cells." Clinical Experimental Allergy 21, no. 5 (September 1991): 632–33. http://dx.doi.org/10.1111/j.1365-2222.1991.tb00863.x.
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McConnell, Kevin W., and Craig M. Coopersmith. "Epithelial cells." Critical Care Medicine 33, Suppl (December 2005): S520—S522. http://dx.doi.org/10.1097/01.ccm.0000187004.09189.1b.
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Davies, R. J., and J. L. Devalia. "Epithelial cells." British Medical Bulletin 48, no. 1 (1992): 85–96. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072544.
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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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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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Durocher, Francine, Jacques Simard, Johanne Ouellette, Virgile Richard, Fernand Labrie, and Georges Pelletier. "Localization of BRCA1 Gene Expression in Adult Cynomolgus Monkey Tissues." Journal of Histochemistry & Cytochemistry 45, no. 9 (September 1997): 1173–88. http://dx.doi.org/10.1177/002215549704500901.
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The breast and ovarian cancer susceptibility gene BRCA1 encodes a phosphoprotein of 1863 amino acids containing a highly conserved N-terminal RING finger domain and a C-terminal acidic region typical of several transcription factors. BRCA1 acts as a tumor suppressor that may inhibit the proliferation of breast and ovarian cancer cells. To gain knowledge and to further understand the biological function of BRCA1, we examined its localization and expression in various tissues from 20-year-old male and female cynomolgus monkeys ( Macaca fascicularis) by in situ hybridization using a 35S-labeled human BRCA1 DNA probe fragment derived from exon 11. In mammary glands, BRCA1 expression was primarily located in the duct and acinar epithelial cells. In the ovary, strong BRCA1 expression was detected in granulosa cells in maturing follicles and in luteal cells of the corpus luteum, as well as in the epithelial cells overlying the tunica albuginea. Specific signal was also observed in epithelial cells of the oviduct, endometrium, cervix, and vagina. Moreover, BRCA1 was strongly expressed in the germinal epithelium of the seminiferous tubules as well as over interstitial cells of the testis, in the epithelium of the epididymis, and in epithelial cells bordering the glandular lumen of the seminal vesicles. Signal was also detected in both the anterior and posterior lobes of the pituitary. In the adrenal glands, the signal was greater in the zona glomerulosa compared to the two other cortical zones, whereas the medullary cells were weakly labeled. In the stomach, and in small and large intestine, epithelial cells of the crypts usually exhibited stronger positive reaction than that observed over surface epithelial lining cells. BRCA1 expression was also found in diverse types of epithelial cells of the thyroid, pancreas, salivary glands, trachea, urinary bladder, and kidneys. In addition to demonstrating widespread tissue- and cell-specific expression of the BRCA1 gene in primate tissues, primarily in the epithelia, we observed a weaker but specific signal in various other cell types, suggesting a generalized biological function of BRCA1.
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Amici, Alessandro W., Fatai O. Onikoyi, and Paola Bonfanti. "Lineage potential, plasticity and environmental reprogramming of epithelial stem/progenitor cells." Biochemical Society Transactions 42, no. 3 (May 22, 2014): 637–44. http://dx.doi.org/10.1042/bst20140047.
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Recent evidence supports and reinforces the concept that environmental cues may reprogramme somatic cells and change their natural fate. In the present review, we concentrate on environmental reprogramming and fate potency of different epithelial cells. These include stratified epithelia, such as the epidermis, hair follicle, cornea and oesophagus, as well as the thymic epithelium, which stands alone among simple and stratified epithelia, and has been shown recently to contain stem cells. In addition, we briefly discuss the pancreas as an example of plasticity of intrinsic progenitors and even differentiated cells. Of relevance, examples of plasticity and fate change characterize pathologies such as oesophageal metaplasia, whose possible cell origin is still debated, but has important implications as a pre-neoplastic event. Although much work remains to be done in order to unravel the full potential and plasticity of epithelial cells, exploitation of this phenomenon has already entered the clinical arena, and might provide new avenues for future cell therapy of these tissues.
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Yankaskas, J. R., J. E. Haizlip, M. Conrad, D. Koval, E. Lazarowski, A. M. Paradiso, C. A. Rinehart, B. Sarkadi, R. Schlegel, and R. C. Boucher. "Papilloma virus immortalized tracheal epithelial cells retain a well-differentiated phenotype." American Journal of Physiology-Cell Physiology 264, no. 5 (May 1, 1993): C1219—C1230. http://dx.doi.org/10.1152/ajpcell.1993.264.5.c1219.
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Human airway epithelial cell lines that retain phenotypic properties representative of the native tissue will be useful physiological models. Human papilloma viral (HPV) genes can immortalize human genital keratinocytes and breast and bronchial epithelia. We transfected cystic fibrosis (CF) and normal tracheobronchial epithelial cell cultures with DNA encoding the HPV-18 E6 and E7 genes and characterized phenotypic properties of resultant cell lines. Of the 11 CF clones isolated, 6 developed a polarized phenotype with vectorial ion transport and membrane-specific expression of histamine and purinergic receptors. The ion transport properties of these lines differed from the normal lines and approximated those of primary CF airway epithelial cell cultures more closely than do those of cell lines transformed with the simian virus 40 large T gene. When transplanted into denuded tracheal grafts, these cells can differentiate into ciliated and secretory phenotypes. We conclude that HPV-18 E6 and E7 genes are sufficient to transform human airway epithelial cells and that the resultant cell lines express differentiated phenotypic properties that approximate those of the native epithelium.
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Sugrue, S. P., and E. D. Hay. "The identification of extracellular matrix (ECM) binding sites on the basal surface of embryonic corneal epithelium and the effect of ECM binding on epithelial collagen production." Journal of Cell Biology 102, no. 5 (May 1, 1986): 1907–16. http://dx.doi.org/10.1083/jcb.102.5.1907.
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Previously, we have shown that embryonic corneal epithelia can interact with, and respond to, soluble extracellular matrices (ECM) (laminin, collagen, and fibronectin). The basal surface of epithelia isolated free of the underlying ECM can be seen to be disrupted by numerous blebs that sprout from this formerly smooth surface. Laminin, collagen, or fibronectin added to the culture medium cause the epithelium to reorganize its cytoskeleton and flatten its basal surface. We show here that ECM molecules at concentrations that reorganize epithelial cytoskeletal morphology also increase the amount of collagen produced by the epithelial cells. However, molecules that do not reorganize basal epithelial morphology (concanavalin A, heparin, bovine serum albumin) have no effect on collagen production. We also report that fluorescently labeled laminin, collagen, and fibronectin, when added to the medium surrounding isolated corneal epithelia, bind to and flatten the basal epithelial cell surface. The binding site on the basal surface is protease sensitive and is specific for each ECM molecule. These results are compatible with the idea that the basal epithelial plasmalemma possesses a diverse population of binding sites for ECM that link cell surface matrix to the cytoskeleton, causing a dramatic cytoskeletal reorganization which in turn results in enhanced production of collagen by the cells.
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Pegtel, Dirk M., Jaap Middeldorp, and David A. Thorley-Lawson. "Epstein-Barr Virus Infection in Ex Vivo Tonsil Epithelial Cell Cultures of Asymptomatic Carriers." Journal of Virology 78, no. 22 (November 15, 2004): 12613–24. http://dx.doi.org/10.1128/jvi.78.22.12613-12624.2004.
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ABSTRACT Epstein-Barr virus (EBV) is found frequently in certain epithelial pathologies, such as nasopharyngeal carcinoma and oral hairy leukoplakia, indicating that the virus can infect epithelial cells in vivo. Recent studies of cell lines imply that epithelial cells may also play a role in persistent EBV infection in vivo. In this report, we show the establishment and characterization of an ex vivo culture model of tonsil epithelial cells, a likely site for EBV infection in vivo. Primary epithelial-cell cultures, generated from tonsil explants, contained a heterogeneous mixture of cells with an ongoing process of differentiation. Keratin expression profiles were consistent with the presence of cells from both surface and crypt epithelia. A small subset of cells could be latently infected by coculture with EBV-releasing cell lines, but not with cell-free virus. We also detected viral-DNA, -mRNA, and -protein expression in cultures from EBV-positive tonsil donors prior to in vitro infection. We conclude that these cells were either already infected at the time of explantation or soon after through cell-to-cell contact with B cells replicating EBV in the explant. Taken together, these findings suggest that the tonsil epithelium of asymptomatic virus carriers is able to sustain EBV infection in vivo. This provides an explanation for the presence of EBV in naso- and oropharyngeal pathologies and is consistent with epithelial cells playing a role in the egress of EBV during persistent infection.
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Egan, Laurence J., Ana de Lecea, Evan D. Lehrman, Gennett M. Myhre, Lars Eckmann, and Martin F. Kagnoff. "Nuclear factor-κB activation promotes restitution of wounded intestinal epithelial monolayers." American Journal of Physiology-Cell Physiology 285, no. 5 (November 2003): C1028—C1035. http://dx.doi.org/10.1152/ajpcell.00167.2003.
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Epithelial restitution, the movement of wound-edge cells into an area of epithelial cell denudation, is an important early step in the ulcer healing process. Growth factors regulate epithelial restitution, yet little is known about the transcriptional pathways that mediate their effects on cell migration. The transcription factor nuclear factor (NF)-κB is a master regulator of the host inflammatory response that is activated in the epithelium in intestinal inflammation, which often accompanies epithelial injury. We hypothesized that NF-κB may be an important transcriptional regulator of epithelial restitution. In an in vitro model of scrape-wounded monolayers of nontransformed rat intestinal epithelial (RIE-1) cells, NF-κB was activated in epithelial cells at the wound edge. Blocking of NF-κB activation by either pharmacological or genetic approaches inhibited intestinal epithelial restitution. Moreover, scrape wounding activated the epidermal growth factor receptor (EGFR) in cells at the wound edge, and, importantly, inhibiting EGFR tyrosine kinase activity decreased scrape wound-induced NF-κB activation and cell migration. These results indicate a novel role of NF-κB activation in a signaling pathway important for restitution and healing of intestinal epithelia. To the extent NF-κB may have parallel functions in vivo, they also suggest a need for caution in the proposed use of NF-κB inhibitors for the treatment of conditions associated with inflammation and injury of intestinal and other mucosal surfaces.
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Watanabe, Kensuke, and Chôsei Kiuna. "Epithelial Damage of Nasal Mucosa in Nasal Allergy." Annals of Otology, Rhinology & Laryngology 107, no. 7 (July 1998): 564–70. http://dx.doi.org/10.1177/000348949810700704.
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Epithelial alterations arising from moderate nasal allergy to house dust were examined and compared to findings in epithelia from nonallergic controls. Biopsy specimens were taken during natural allergen exposure from two different sites: 1) the anterior tip of the inferior turbinate and 2) 2 cm behind it. The tissues were examined by both electron and light microscopy. In the allergic group, epithelial damage was found to be remarkable in the anterior nasal mucosae, where nonciliated cells were prevalent, but minor in the posterior nasal mucosae comprising ciliated and goblet cells. In the anterior nasal mucosae, conspicuous intercellular edema, epithelial shedding, and clusters of eosinophils in the epithelial layer were observed, whereas only a little epithelial shedding and edema in the basal area of the epithelium was noted in the ciliated areas. In controls, pathologic changes were not observed, although a little epithelial shedding was seen in the anterior turbinate. Although there are arguments for and against epithelial shedding in nasal allergy, this study confirms its presence even in patients with moderate allergy.
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Ludlow, Martin, Rory D. de Vries, Ken Lemon, Stephen McQuaid, Emma Millar, Geert van Amerongen, Selma Yüksel, et al. "Infection of lymphoid tissues in the macaque upper respiratory tract contributes to the emergence of transmissible measles virus." Journal of General Virology 94, no. 9 (September 1, 2013): 1933–44. http://dx.doi.org/10.1099/vir.0.054650-0.
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Measles virus (MV), a member of the family Paramyxoviridae, remains a major cause of morbidity and mortality in the developing world. MV is spread by aerosols but the mechanism(s) responsible for the high transmissibility of MV are largely unknown. We previously infected macaques with enhanced green fluorescent protein-expressing recombinant MV and euthanized them at a range of time points. In this study a comprehensive pathological analysis has been performed of tissues from the respiratory tract around the peak of virus replication. Isolation of virus from nose and throat swab samples showed that high levels of both cell-associated and cell-free virus were present in the upper respiratory tract. Analysis of tissue sections from lung and primary bronchus revealed localized infection of epithelial cells, concomitant infiltration of MV-infected immune cells into the epithelium and localized shedding of cells or cell debris into the lumen. While high numbers of MV-infected cells were present in the tongue, these were largely encapsulated by intact keratinocyte cell layers that likely limit virus transmission. In contrast, the integrity of tonsillar and adenoidal epithelia was disrupted with high numbers of MV-infected epithelial cells and infiltrating immune cells present throughout epithelial cell layers. Disruption was associated with large numbers of MV-infected cells or cell debris ‘spilling’ from epithelia into the respiratory tract. The coughing and sneezing response induced by disruption of the ciliated epithelium, leading to the expulsion of MV-infected cells, cell debris and cell-free virus, contributes to the highly infectious nature of MV.
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Amano, K., K. Miyake, J. L. Borke, and P. L. McNeil. "Breaking Biological Barriers with a Toothbrush." Journal of Dental Research 86, no. 8 (August 2007): 769–74. http://dx.doi.org/10.1177/154405910708600816.
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Toothbrushing exposes epithelia and other tissues of the oral cavity to mechanical stress. Here, we investigated whether brushing induces cell wounding—plasma membrane disruption—in epithelial and other cell types in the oral cavity. Brushing of the gingivae and tongues of rats resulted in a striking increase in the number of cells positive for a marker of disruption injury. These cells included those in all strata of the gingival epithelium, and in the skeletal muscle of the tongue. Additionally, we found that brushing resulted in an increase in c-fos expression by junctional epithelial and skeletal muscle cells. Epithelial barrier function, however, was not overtly affected by brushing, despite the observed individual injuries to cells. We concluded that brushing disrupts cell plasma membrane barriers in the oral cavity and activates gene expression events that may lead to local adaptive changes in tissue architecture beneficial to gingival health.
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Ghosh, Baishakhi, Bongsoo Park, Debarshi Bhowmik, Kristine Nishida, Molly Lauver, Nirupama Putcha, Peisong Gao, et al. "Strong correlation between air-liquid interface cultures and in vivo transcriptomics of nasal brush biopsy." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 5 (May 1, 2020): L1056—L1062. http://dx.doi.org/10.1152/ajplung.00050.2020.
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Air-liquid interface (ALI) cultures are ex vivo models that are used extensively to study the epithelium of patients with chronic respiratory diseases. However, the in vitro conditions impose a milieu different from that encountered in the patient in vivo, and the degree to which this alters gene expression remains unclear. In this study we employed RNA sequencing to compare the transcriptome of fresh brushings of nasal epithelial cells with that of ALI-cultured epithelial cells from the same patients. We observed a strong correlation between cells cultured at the ALI and cells obtained from the brushed nasal epithelia: 96% of expressed genes showed similar expression profiles, although there was greater similarity between the brushed samples. We observed that while the ALI model provides an excellent representation of the in vivo airway epithelial transcriptome for mechanistic studies, several pathways are affected by the change in milieu.
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Liu, June, Laura E. Pascal, Sudhir Isharwal, Daniel Metzger, Raquel Ramos Garcia, Jan Pilch, Susan Kasper, et al. "Regenerated Luminal Epithelial Cells Are Derived from Preexisting Luminal Epithelial Cells in Adult Mouse Prostate." Molecular Endocrinology 25, no. 11 (November 1, 2011): 1849–57. http://dx.doi.org/10.1210/me.2011-1081.
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Abstract Determining the source of regenerated luminal epithelial cells in the adult prostate during androgen deprivation and replacement will provide insights into the origin of prostate cancer cells and their fate during androgen deprivation therapy. Prostate stem cells in the epithelial layer have been suggested to give rise to luminal epithelium. However, the extent of stem cell participation to prostate regrowth is not clear. In this report, using prostate-specific antigen-CreERT2-based genetic lineage marking/tracing in mice, preexisting luminal epithelial cells were shown to be a source of regenerated luminal epithelial cells in the adult prostate. Prostatic luminal epithelial cells could survive androgen deprivation and were capable of proliferating upon androgen replacement. Prostate cancer cells, typically exhibiting a luminal epithelial phenotype, may retain this intrinsic capability to survive and regenerate in response to changes in androgen signaling, providing part of the mechanism for the ultimate failure of androgen deprivation therapy in prostate cancer.
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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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Longphre, M., L. Y. Zhang, J. R. Harkema, and S. R. Kleeberger. "Mass cells contribute to O3-induced epithelial damage and proliferation in nasal and bronchial airways of mice." Journal of Applied Physiology 80, no. 4 (April 1, 1996): 1322–30. http://dx.doi.org/10.1152/jappl.1996.80.4.1322.
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Ozone (O3) exposure produces inflammation in the airways of humans and animal models. However, the mechanism by which O3 affects these changes is uncertain. Mast cells are strategically located below the epithelium of the airways and are capable of releasing a number of proinflammatory mediators. We tested the hypothesis that mast cells contribute to inflammation, epithelial sloughing, and epithelial proliferation in the nasal and terminal bronchiolar murine airways after O3 exposure. Mast cell-sufficient (+/+), mast cell-deficient (W/Wv), and mast cell-repleted [bone marrow-transplanted (BMT) W/Wv] mice were exposed to 2 ppm O3 or filtered air for 3 h. Nasal and bronchoalveolar lavage fluids were collected 6 and 24 h after exposure. Differential cell counts and protein content of the lavage fluids were used as indicators of inflammation and permeability changes in the airways. O3-induced epithelial injury was assessed by light microscopy, and O3-induced DNA synthesis in airway epithelium was estimated by using a 5-bromo-2′-deoxyuridine-labeling index in the nasal and terminal bronchiolar epithelia. Relative to air control mice, O3 caused significant increases in inflammation, epithelial injury, and epithelial DNA synthesis in +/+ mice. There was no significant effect of O3 exposure on any measured parameter in the W/Wv mice. To further assess the role of mast cells in O3-induced epithelial damage, mast cells were restored in W/Wv mice by BMT from +/+ congeners. Relative to sham-transplanted W/Wv mice, O3 caused significant increases in epithelial damage and DNA synthesis as well as inflammatory indicators in BMT W/Wv mice. These observations are consistent with the hypothesis that mast cells significantly modulate the inflammatory and proliferative responses of the murine airways to O3.
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FERNANDES, M. N., and S. A. PERNA-MARTINS. "Epithelial gill cells in the armored catfish, Hypostomus cf. plecostomus (Loricariidae)." Revista Brasileira de Biologia 61, no. 1 (February 2001): 69–78. http://dx.doi.org/10.1590/s0034-71082001000100010.
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Epithelial gill cell morphology and distribution were investigated in the armored catfish, Hypostomus cf. plecostomus, which lives in soft ion-poor Brazilian freshwaters. Pavement cells are the most abundant type of cell on both filament and lamellar epithelia and there are a great number of mucous and chloride cells between them. Mucous cells are almost covered by adjacent pavement cells and have large packed granules showing electrondense differences. No mucous cells were found on the lamellar epithelium. Chloride cell were distributed throughout both epithelia and usually have large apical surface facing the external medium and may exhibit short and sparsely distributed microvilli. The presence of chloride cells on the lamellar epithelium may be an adaptation to low ion concentrations in the water, allowing for improved ion-transport capacity of the gill. The large size of these cells increases the water-blood barrier and may affect the transference of respiratory gases. However, the negative effect on the respiratory process may be minimized by this species' ability to resort to atmospheric air to fulfill its oxygen requirements.
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Swarnameenakshi, S., and Nithyajagannathan Nithyajagannathan. "Cytomorphometric Analysis of Oral Epithelial Cells in Menstrual Cycle." International Journal of Pharma Research and Health Sciences 5, no. 3 (2017): 1695–97. http://dx.doi.org/10.21276/ijprhs.2017.03.02.
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Takito, Jiro, and Qais Al-Awqati. "Conversion of ES cells to columnar epithelia by hensin and to squamous epithelia by laminin." Journal of Cell Biology 166, no. 7 (September 27, 2004): 1093–102. http://dx.doi.org/10.1083/jcb.200405159.
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Single-layered epithelia are the first differentiated cell types to develop in the embryo, with columnar and squamous types appearing immediately after blastocyst implantation. Here, we show that mouse embryonic stem cells seeded on hensin or laminin, but not fibronectin or collagen type IV, formed hemispheric epithelial structures whose outermost layer terminally differentiated to an epithelium that resembled the visceral endoderm. Hensin induced columnar epithelia, whereas laminin formed squamous epithelia. At the egg cylinder stage, the distal visceral endoderm is columnar, and these cells begin to migrate anteriorly to create the anterior visceral endoderm, which assumes a squamous shape. Hensin expression coincided with the dynamic appearance and disappearance of columnar cells at the egg cylinder stage of the embryo. These expression patterns, and the fact that hensin null embryos (and those already reported for laminin) die at the onset of egg cylinder formation, support the view that hensin and laminin are required for terminal differentiation of columnar and squamous epithelial phenotypes during early embryogenesis.
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Coraux, Christelle, Aurélie Delplanque, Jocelyne Hinnrasky, Bruno Peault, Edith Puchelle, and Dominique Gaillard. "Distribution of Integrins During Human Fetal Lung Development." Journal of Histochemistry & Cytochemistry 46, no. 7 (July 1998): 803–10. http://dx.doi.org/10.1177/002215549804600703.
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Interactions between epithelial cells and the extracellular matrix through integrins play a key role in the development of the lung by modulating branching morphogenesis, epithelial cell polarization, and differentiation. To determine the role of integrins during the different stages of lung development, we investigated the distribution of eight integrin subunits in the trachea and lung from human fetuses. In distal airways, during the early pseudoglandular stage of development, the α2-, α5-, α6-, αv-, and β1-subunits were detected in all epithelial cell plasma membranes, and polarized but undifferentiated tracheal epithelial cells expressed α3-, α6-, and β1-subunits in the plasma membrane of the cells facing the basement membrane. The α6- and β4-chains were detected along the basal plasma membrane of the basal cells in differentiated tracheal epithelia. The α4-subunit was detected in all respiratory cells throughout fetal development. In the submucosal glands, myoepithelial cells expressed the integrin subunits found in the undifferentiated cells of the developing airways, whereas the secretory cells expressed only α2-, α3-, α4-, α6-, and β1-subunits. These results demonstrate differential expression of integrins during lung development and suggest that integrins may play multiple roles in organogenesis and maturation of respiratory surface epithelium and glands.