Academic literature on the topic 'Epithelium Cell differentiation. Keratin Epithelium Keratin Cell Differentiation'
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Journal articles on the topic "Epithelium Cell differentiation. Keratin Epithelium Keratin Cell Differentiation"
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Pang, Y. Y., A. Schermer, J. Yu, and T. T. Sun. "Suprabasal change and subsequent formation of disulfide-stabilized homo- and hetero-dimers of keratins during esophageal epithelial differentiation." Journal of Cell Science 104, no. 3 (March 1, 1993): 727–40. http://dx.doi.org/10.1242/jcs.104.3.727.
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Rabbit esophageal epithelium, a parakeratinized stratified epithelium, synthesizes as one of its major differentiation products a keratin pair consisting of a basic K4 (59 kDa) and an acidic K13 (41 kDa) keratin. Although immunohistochemical staining data suggest that in esophageal epithelia of some other species these two keratins are suprabasally located, antigenic masking of the epitopes in the basal cells has not been ruled out. Using several well-characterized monoclonal antibodies including AE8, which specifically recognizes K13, coupled with biochemical analysis of keratins of basal and suprabasal cells isolated from confluent rabbit esophageal epithelial culture, we have obtained direct evidence that K4 and K13 keratins are largely absent in the undifferentiated basal cells, but are present in large amounts in suprabasal cells. We also show that in the cornified cell layers that are formed during the terminal stage of esophageal epithelial differentiation, K4 and K13 keratins become disulfide-crosslinked to form three different dimers. Two of them (110 kDa and 100 kDa) are heterodimers and consist of equimolar amounts of K4 and K13; they presumably represent isomers crosslinked via different cysteine residues. The third dimer (90 kDa) was found to be a homodimer of the acidic K13 keratin. Trypsinization experiment established that at least some of the disulfide crosslinks in the K4/K13 heterodimer must involve cysteine residues residing in the trypsin-resistant rod domains of keratins. Air-oxidation of in vitro reconstituted filaments reproduced the two heterodimers, which most likely involve the crosslinking between type I and type II keratins of different coiled coils. The formation of these disulfide-crosslinked keratin dimers, instead of higher molecular mass oligomers or polymers as occurring in the epidermis and hair, may contribute to the formation of cornified cells with a physical stability and rigidity that are optimal for esophageal function. Our data also suggest that interactions involved in the formation of homodimers, thought to be metastable and unimportant during the initial step of filament assembly (i.e. tetramer formation), may actually play an important role in stabilizing a higher order structure in mature keratin filaments.
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Schermer, A., S. Galvin, and T. T. Sun. "Differentiation-related expression of a major 64K corneal keratin in vivo and in culture suggests limbal location of corneal epithelial stem cells." Journal of Cell Biology 103, no. 1 (July 1, 1986): 49–62. http://dx.doi.org/10.1083/jcb.103.1.49.
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In this paper we present keratin expression data that lend strong support to a model of corneal epithelial maturation in which the stem cells are located in the limbus, the transitional zone between cornea and conjunctiva. Using a new monoclonal antibody, AE5, which is highly specific for a 64,000-mol-wt corneal keratin, designated RK3, we demonstrate that this keratin is localized in all cell layers of rabbit corneal epithelium, but only in the suprabasal layers of the limbal epithelium. Analysis of cultured corneal keratinocytes showed that they express sequentially three major keratin pairs. Early cultures consisting of a monolayer of "basal" cells express mainly the 50/58K keratins, exponentially growing cells synthesize additional 48/56K keratins, and postconfluent, heavily stratified cultures begin to express the 55/64K corneal keratins. Cell separation experiments showed that basal cells isolated from postconfluent cultures contain predominantly the 50/58K pair, whereas suprabasal cells contain additional 55/64K and 48/56K pairs. Basal cells of the older, postconfluent cultures, however, can become AE5 positive, indicating that suprabasal location is not a prerequisite for the expression of the 64K keratin. Taken together, these results suggest that the acidic 55K and basic 64K keratins represent markers for an advanced stage of corneal epithelial differentiation. The fact that epithelial basal cells of central cornea but not those of the limbus possess the 64K keratin therefore indicates that corneal basal cells are in a more differentiated state than limbal basal cells. These findings, coupled with the known centripetal migration of corneal epithelial cells, strongly suggest that corneal epithelial stem cells are located in the limbus, and that corneal basal cells correspond to "transient amplifying cells" in the scheme of "stem cells----transient amplifying cells----terminally differentiated cells."
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Nicolas, J. F., W. Savino, A. Reano, J. Viac, J. Brochier, and M. Dardenne. "Heterogeneity of thymic epithelial cell (TEC) keratins--immunohistochemical and biochemical evidence for a subset of highly differentiated TEC in the mouse." Journal of Histochemistry & Cytochemistry 33, no. 7 (July 1985): 687–94. http://dx.doi.org/10.1177/33.7.2409128.
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The mouse thymic epithelial network was studied using three different anti-keratin antibodies. One of these antibodies, KL1, exclusively recognized a small subset of medullary epithelial cells characterized by its content of a high molecular weight keratin (63 kD). Since epithelial differentiation is known to be associated with the acquisition of high molecular weight keratins, KL1-positive cells, which express the Ia antigen and secrete thymulin, may represent a subset of highly differentiated cells among mouse thymic epithelial cells (TEC). These data reflect the heterogeneity of the thymic epithelium and support the concept that distinct TEC subsets might provide the thymus with different microenvironments.
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Divani, Smaroula, and George Kalodimos. "Expression of cytokeratins 8 and 17 as a diagnostic marker of cervical intraepithelial neoplasia." Archive of Oncology 18, no. 3 (2010): 88–90. http://dx.doi.org/10.2298/aoo1003088d.
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Cytokeratins belong to the most fundamental markers of epithelial differentiation. Their composition reflects both a cell type and the differentiation status. The aim of this study was to investigate the expression of keratins 8 and 17 in normal cervical epithelium, mature and immature metaplastic epithelium as well as in various grades of intraepithelial neoplasia and squamous cell carcinomas. Fifty-eight smears representing 20 normal, 23 LGSILs, 12 HGSILs and 3 cervical carcinomas were stained with anticytokeratin 8 (clone 35bH11) and anticytokeratin 17 (clone Ks17E3). Expression of both keratins was examined and the percentages of immunoreactive normal, metaplastic, intraepithelial neoplastic and malignant cells were determined. Evaluation of tissue sections was also performed. Keratin 17 was identified in all SILs and carcinomas. It was also present in 3/20 (15%) of normal cervical smears that contained immature metaplastic cells. Keratin 8 was found in the majority of LGSIL cases 20/23 (86.9%), in all HGSIL and malignant lesions as well as in endocervical columnar epithelial cells and in 5/20 (25%) normal smears with immature metaplastic cells. Both keratins showed a more extensive and intense expression in severe lesions. Evaluation of tissue sections revealed expression of CK8 and CK17 of various intensity in most of the premalignant and malignant cases. Premalignant and malignant cells showed similarities in cytokeratins 8 and 17 expression. Both CKs were not expressed in normal ectocervical epithelium. The study of the expression of CK8 and CK17 may contribute in detection of cervical intraepithelial neoplasia.
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Radoja, Nadezda, Mayumi Komine, Sang H. Jho, Miroslav Blumenberg, and Marjana Tomic-Canic. "Novel Mechanism of Steroid Action in Skin through Glucocorticoid Receptor Monomers." Molecular and Cellular Biology 20, no. 12 (June 15, 2000): 4328–39. http://dx.doi.org/10.1128/mcb.20.12.4328-4339.2000.
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ABSTRACT Glucocorticoids (GCs), important regulators of epidermal growth, differentiation, and homeostasis, are used extensively in the treatment of skin diseases. Using keratin gene expression as a paradigm of epidermal physiology and pathology, we have developed a model system to study the molecular mechanism of GCs action in skin. Here we describe a novel mechanism of suppression of transcription by the glucocorticoid receptor (GR) that represents an example of customizing a device for transcriptional regulation to target a specific group of genes within the target tissue, in our case, epidermis. We have shown that GCs repress the expression of the basal-cell-specific keratins K5 and K14 and disease-associated keratins K6, K16, and K17 but not the differentiation-specific keratins K3 and K10 or the simple epithelium-specific keratins K8, K18, and K19. We have identified the negative recognition elements (nGREs) in all five regulated keratin gene promoters. Detailed footprinting revealed that the function of nGREs is to instruct the GR to bind as four monomers. Furthermore, using cotransfection and antisense technology we have found that, unlike SRC-1 and GRIP-1, which are not involved in the GR complex that suppresses keratin genes, histone acetyltransferase and CBP are. In addition, we have found that GR, independently from GREs, blocks the induction of keratin gene expression by AP1. We conclude that GR suppresses keratin gene expression through two independent mechanisms: directly, through interactions of keratin nGREs with four GR monomers, as well as indirectly, by blocking the AP1 induction of keratin gene expression.
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Castro-Munozledo, F. "Development of a spontaneous permanent cell line of rabbit corneal epithelial cells that undergoes sequential stages of differentiation in cell culture." Journal of Cell Science 107, no. 8 (August 1, 1994): 2343–51. http://dx.doi.org/10.1242/jcs.107.8.2343.
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Established epithelial cell lines that retain their differentiation potential and growth regulatory characteristics can provide valuable tools for studying gene regulation, extracellular matrix synthesis or growth factor response. They are also useful for drug development and toxicity testing. Experiments were therefore carried out to optimize culture conditions for the long-term, serial transfer of corneal epithelial cells in the presence of 3T3 feeder layers; and to establish a permanent cell line. In such experiments, rabbit corneal epithelial cells were seeded at low inoculation densities, and transferred every 5 days. After 80 population doublings, an epithelial cell line, RCE1, emerged. The cell line is heteroploid, with an average population doubling time of 15.5 hours (vs 18 hours for primary cultures). When RCE1 cells reached confluence, they stratified to form a three- to five-layered epithelium and expressed the differentiation-related keratin pair K3/K12 as shown by immunoblot and immunostaining. Biosynthetic labeling of proliferating, confluent and stratified cultures further showed that RCE1 cells expressed keratin pairs K5/K14, K6/K16 and K3/K12, thus mimicking faithfully the stage-dependent differentiation of primary cultures of rabbit corneal keratinocytes. The results demonstrated that RCE1 cells provide a useful model for studying corneal cell growth and differentiation.
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Miyagawa, Shinichi, and Taisen Iguchi. "Epithelial estrogen receptor 1 intrinsically mediates squamous differentiation in the mouse vagina." Proceedings of the National Academy of Sciences 112, no. 42 (October 5, 2015): 12986–91. http://dx.doi.org/10.1073/pnas.1513550112.
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Estrogen-mediated actions in female reproductive organs are tightly regulated, mainly through estrogen receptor 1 (ESR1). The mouse vaginal epithelium cyclically exhibits cell proliferation and differentiation in response to estrogen and provides a unique model for analyzing the homeostasis of stratified squamous epithelia. To address the role of ESR1-mediated tissue events during homeostasis, we analyzed mice with a vaginal epithelium-specific knockout of Esr1 driven by keratin 5-Cre (K5-Esr1KO). We show here that loss of epithelial ESR1 in the vagina resulted in aberrant epithelial cell proliferation in the suprabasal cell layers and led to failure of keratinized differentiation. Gene expression analysis showed that several known estrogen target genes, including erbB growth factor ligands, were not induced by estrogen in the K5-Esr1KO mouse vagina. Organ culture experiments revealed that the addition of erbB growth factor ligands, such as amphiregulin, could activate keratinized differentiation in the absence of epithelial ESR1. Thus, epithelial ESR1 integrates estrogen and growth factor signaling to mediate regulation of cell proliferation in squamous differentiation, and our results provide new insights into estrogen-mediated homeostasis in female reproductive organs.
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Rentrop, M., B. Knapp, H. Winter, and J. Schweizer. "Differential localization of distinct keratin mRNA-species in mouse tongue epithelium by in situ hybridization with specific cDNA probes." Journal of Cell Biology 103, no. 6 (December 1, 1986): 2583–91. http://dx.doi.org/10.1083/jcb.103.6.2583.
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The tongue of the adult mouse is covered by a multilayered squamous epithelium which is continuous on the ventral surface, however interrupted on the dorsal surface by many filiform and few fungiform papillae. The filiform papillae themselves are subdivided into an anterior and posterior unit exhibiting different forms of keratinization. Thus, the entire epithelium shows a pronounced morphological diversity of well recognizable tissue units. We have used a highly sensitive in situ hybridization technique to investigate the differential expression of keratin mRNAs in the tongue epithelium. The hybridization probes used were cDNA restriction fragments complementary to the most specific 3'-regions of any given keratin mRNA. We could show that independent of the morphologically different tongue regions, all basal cells uniformly express the mRNA of a type I 52-kD keratin, typical also for basal cells of the epidermis. Immediately above the homogenous basal layer a vertically oriented specialization of the keratin expression occurs within the morphological tissue units. Thus the dorsal interpapillary and ventral epithelium express the mRNAs of a type II 57-kD and a type I 47-kD keratin pair. In contrast, in the anterior unit of the filiform papillae, only the 47-kD mRNA is present, indicating that this keratin may be coexpressed in tongue epithelium with different type II partners. In suprabasal cells of both, the fungiform papillae and the posterior unit of the filiform papillae, a mRNA of a type I 59-kD keratin could be detected; however, its type II 67-kD epidermal counterpart seems not to be present in these cells. Most surprisingly, in distinct cells of both types of papillae, a type I 50-kD keratin mRNA could be localized which usually is associated with epidermal hyperproliferation. In conclusion, the in situ hybridization technique applied has been proved to be a powerful method for detailed studies of differentiation processes, especially in morphologically complex epithelia.
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Pan, Jie, and Nelly Auersperg. "Spatiotemporal changes in cytokeratin expression in the neonatal rat ovary." Biochemistry and Cell Biology 76, no. 1 (February 1, 1998): 27–35. http://dx.doi.org/10.1139/o98-002.
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Ovarian granulosa cells are derived embryologically from two keratin-positive epithelia of mesodermal origin, the ovarian rete and the ovarian surface epithelium. In the rat, presumptive granulosa cells still express keratin at birth but as they acquire functions related to oocyte support and steroidogenesis in the maturing ovary they lose this epithelial differentiation marker. Using double-label immunofluorescence microscopy, we examined the distribution of keratin-expressing granulosa cells in rat ovaries on days 1-10 postpartum in relation to (i) laminin and collagen type IV in follicular basement membranes, (ii) the zona pellucida, and (iii) 3β-hydroxysteroid dehydrogenase activity. Keratin was present in most (pre)granulosa cells on days 1-3. As the cells became multilayered in growing follicles, keratin was retained by granulosa cells adjacent to follicular basement membranes but disappeared from cells that were displaced towards follicular centers. From day 7 on, large follicles lacked keratin altogether. Laminin was a consistent component of follicular basement membranes at all ages, while collagen IV varied and diminished in parallel with keratin. 3β-Hydroxysteroid dehydrogenase was demonstrable in stromal interstitial cells from day 7 on. Zona pellucida first appeared in primary follicles adjacent to keratin-positive cells and subsequently became surounded with keratin-negative granulosa cells in growing follicles. The results suggest different roles for laminin and collagen IV in follicular basement membranes and support the hypothesis that keratin expression by granulosa cells depends on paracrine interactions with the ovarian stroma. In early growing follicles, these interactions may be interrupted by physical removal from the vicinity of the basement membranes as the granulosa cells become multilayered. In the more mature follicles, the loss of keratin from all granulosa cells suggests that the required stromal signals cease, perhaps as the perifollicular stroma differentiates into the theca.Key words: ovary, differentiation, keratin, basal membrane, development.
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Boukamp, P., J. Chen, F. Gonzales, P. A. Jones, and N. E. Fusenig. "Progressive stages of "transdifferentiation" from epidermal to mesenchymal phenotype induced by MyoD1 transfection, 5-aza-2'-deoxycytidine treatment, and selection for reduced cell attachment in the human keratinocyte line HaCaT." Journal of Cell Biology 116, no. 5 (March 1, 1992): 1257–71. http://dx.doi.org/10.1083/jcb.116.5.1257.
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The ability of the myogenic determination gene (MyoD1) to convert differentiating human keratinocytes (HaCaT cell-line) to the myogenic pathway and the effect of MyoD1 on the epidermal phenotype was studied in culture and in surface transplants on nude mice. MyoD1 transfection induced the synthesis of myosin, desmin, and vimentin without substantially altering the epidermal differentiation properties (morphology, keratin profile) in vitro nor epidermal morphogenesis (formation of a complex stratified squamous epithelium) in surface transplants, demonstrating the stability of the keratinocyte phenotype. 5-Aza-CdR treatment of these MyoD1-transfected cells had little effect on the cultured cells but a morphologically unstructured epithelium was formed with no indications of typical cell layers including cornification. Since prevention of epidermal strata in transplants was not accompanied by blocked epidermal differentiation markers (keratins K1 and K10, involucrin, and filaggrin), the dissociation of morphogenesis and expression of these markers argues for independently controlled processes. A subpopulation of less adhesive cells, isolated from the 5-aza-CdR treated MyoD1-transfectants, had lost most epithelial characteristics in culture (epidermal keratins, desmosomal proteins, and surface-glycoprotein Gp90) and had shifted to a mesenchymal/myogenic phenotype (fibroblastic morphology, transactivation of Myf3 and myogenin, expression of myosin, desmin, vimentin, and Gp130). Moreover, the cells had lost the ability to stratify and remained as a monolayer of flat elongated cells in transplants. These subsequent changes from a fully differentiated keratinocyte to a mesenchymal/myogenic phenotype strongly argue for a complex "transdifferentiation" process which occurred in the original monoclonal human epidermal HaCaT cells.
Dissertations / Theses on the topic "Epithelium Cell differentiation. Keratin Epithelium Keratin Cell Differentiation"
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Turunen, Denise E. "Immunologic identification of sulcular epithelial differentiation antigens in cytology preparations a thesis submitted in partial fulfillment ... periodontics ... /." 1989. http://books.google.com/books?id=FFM_AAAAMAAJ.
Full textBook chapters on the topic "Epithelium Cell differentiation. Keratin Epithelium Keratin Cell Differentiation"
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Roop, Dennis R. "Chapter 9 Regulation of Keratin Gene Expression During Differentiation of Epidermal and Vaginal Epithelial Cells." In The Molecular and Developmental Biology of Keratins, 195–207. Elsevier, 1987. http://dx.doi.org/10.1016/s0070-2153(08)60104-0.
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