Relevant bibliographies by topics / Epithelium Cell differentiation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Epithelium Cell differentiation'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Epithelium Cell differentiation"

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Levine, J. F., and F. E. Stockdale. "Cell-cell interactions promote mammary epithelial cell differentiation." Journal of Cell Biology 100, no. 5 (May 1, 1985): 1415–22. http://dx.doi.org/10.1083/jcb.100.5.1415.

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Mammary epithelium differentiates in a stromal milieu of adipocytes and fibroblasts. To investigate cell-cell interactions that may influence mammary epithelial cell differentiation, we developed a co-culture system of murine mammary epithelium and adipocytes and other fibroblasts. Insofar as caseins are specific molecular markers of mammary epithelial differentiation, rat anti-mouse casein monoclonal antibodies were raised against the three major mouse casein components to study this interaction. Mammary epithelium from mid-pregnant mice was plated on confluent irradiated monolayers of 3T3-L1 cells, a subclone of the Swiss 3T3 cell line that differentiates into adipocytes in monolayer culture and other cell monolayers (3T3-C2 cells, Swiss 3T3 cells, and human foreskin fibroblasts). Casein was synthesized by mammary epithelium only in the presence of co-cultured cells and the lactogenic hormone combination of insulin, hydrocortisone, and prolactin. Synthesis and accumulation of alpha-, beta-, and gamma-mouse casein within the epithelium was shown by immunohistochemical staining of cultured cells with anti-casein monoclonal antibodies, and the specificity of the immunohistochemical reaction was demonstrated using immunoblots. A competitive immunoassay was used to measure the amount of casein secreted into the culture medium. In a 24-h period, mammary epithelium co-cultured with 3T3-L1 cells secreted 12-20 micrograms beta-casein per culture dish. There was evidence of specificity in the cell-cell interaction that mediates hormone-dependent casein synthesis. Swiss 3T3 cells, newborn foreskin fibroblasts, substrate-attached material ("extracellular matrix"), and tissue culture plastic did not support casein synthesis, whereas monolayers of 3T3-L1 and 3T3-C2 cells, a subclone of Swiss 3T3 cells that does not undergo adipocyte differentiation, did. We conclude that interaction between mammary epithelium and other specific nonepithelial cells markedly influences the acquisition of hormone sensitivity of the epithelium and hormone-dependent differentiation.
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Yang, Honghua, Min Min Lu, Lili Zhang, Jeffrey A. Whitsett, and Edward E. Morrisey. "GATA6 regulates differentiation of distal lung epithelium." Development 129, no. 9 (May 1, 2002): 2233–46. http://dx.doi.org/10.1242/dev.129.9.2233.

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GATA6 is a member of the GATA family of zinc-finger transcriptional regulators and is the only known GATA factor expressed in the distal epithelium of the lung during development. To define the role that GATA6 plays during lung epithelial cell development, we expressed a GATA6-Engrailed dominant-negative fusion protein in the distal lung epithelium of transgenic mice. Transgenic embryos lacked detectable alveolar epithelial type 1 cells in the distal airway epithelium. These embryos also exhibited increased Foxp2 gene expression, suggesting a disruption in late alveolar epithelial differentiation. Alveolar epithelial type 2 cells, which are progenitors of alveolar epithelial type 1 cells, were correctly specified as shown by normal thyroid transcription factor 1 and surfactant protein A gene expression. However, attenuated endogenous surfactant protein C expression indicated that alveolar epithelial type 2 cell differentiation was perturbed in transgenic embryos. The number of proximal airway tubules is also reduced in these embryos, suggesting a role for GATA6 in regulating distal-proximal airway development. Finally, a functional role for GATA factor function in alveolar epithelial type 1 cell gene regulation is supported by the ability of GATA6 to trans-activate the mouse aquaporin-5 promoter. Together, these data implicate GATA6 as an important regulator of distal epithelial cell differentiation and proximal airway development in the mouse.
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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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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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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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Smiley-Jewell, Suzette M., Susan J. Nishio, Alison J. Weir, and Charles G. Plopper. "Neonatal Clara cell toxicity by 4-ipomeanol alters bronchiolar organization in adult rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 4 (April 1, 1998): L485—L498. http://dx.doi.org/10.1152/ajplung.1998.274.4.l485.

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Nonciliated bronchiolar (Clara) cells metabolize environmental toxicants, are progenitor cells during development, and differentiate postnatally. Because differentiating Clara cells of neonatal rabbits are injured at lower doses by the cytochrome P-450-activated cytotoxicant 4-ipomeanol than are those of adults, the impact of early injury on the bronchiolar epithelial organization of adults was defined by treating neonates (3–21 days) and examining them at 4–6 wk. Bronchiolar epithelium of 6-wk-old animals treated on day 7 was most altered from that of control animals. Almost 100% of the bronchioles were lined by zones of squamous epithelial cells. Compared with control animals, the distal bronchiolar epithelium of 4-ipomeanol-treated animals had more squamous cells (70–90 vs. 0%) with a reduced overall epithelial thickness (25% of control value), fewer ciliated cells (0 vs. 10–20%), a reduced expression of Clara cell markers of differentiation (cytochrome P-4502B, NADPH reductase, and 10-kDa protein), and undifferentiated nonciliated cuboidal cell ultrastructure. We conclude that early injury to differentiating rabbit Clara cells by a cytochrome P-450-mediated toxicant inhibits bronchiolar epithelial differentiation and greatly affects repair.
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Cui, Yongzhi, Greg Riedlinger, Keiko Miyoshi, Wei Tang, Cuiling Li, Chu-Xia Deng, Gertraud W. Robinson, and Lothar Hennighausen. "Inactivation of Stat5 in Mouse Mammary Epithelium during Pregnancy Reveals Distinct Functions in Cell Proliferation, Survival, and Differentiation." Molecular and Cellular Biology 24, no. 18 (September 15, 2004): 8037–47. http://dx.doi.org/10.1128/mcb.24.18.8037-8047.2004.

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ABSTRACT This study explored the functions of the signal transducers and activators of transcription 5a and 5b (referred to as Stat5 here) during different stages of mouse mammary gland development by using conditional gene inactivation. Mammary gland morphogenesis includes cell specification, proliferation and differentiation during pregnancy, cell survival and maintenance of differentiation throughout lactation, and cell death during involution. Stat5 is activated by prolactin, and its presence is mandatory for the proliferation and differentiation of mammary epithelium during pregnancy. To address the question of whether Stat5 is also necessary for the maintenance and survival of the differentiated epithelium, the two genes were deleted at different time points. The 110-kb Stat5 locus in the mouse was bracketed with loxP sites, and its deletion was accomplished by using two Cre-expressing transgenic lines. Loss of Stat5 prior to pregnancy prevented epithelial proliferation and differentiation. Deletion of Stat5 during pregnancy, after mammary epithelium had entered Stat5-mediated differentiation, resulted in premature cell death, indicating that at this stage epithelial cell proliferation, differentiation, and survival require Stat5.
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Caniggia, I., I. Tseu, R. N. Han, B. T. Smith, K. Tanswell, and M. Post. "Spatial and temporal differences in fibroblast behavior in fetal rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 6 (December 1, 1991): L424—L433. http://dx.doi.org/10.1152/ajplung.1991.261.6.l424.

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Fibroblast-epithelial interactions were investigated in cells from late-gestation fetal rat lung. Fibroblasts from the pseudoglandular stage of lung development stimulated epithelial cell proliferation, whereas fibroblasts from the saccular stage promoted epithelial cell differentiation. The developmental switch from proliferation to differentiation seemed to be controlled by both cell types. Fibroblast-derived epithelial cell growth-promoting activity, evident in cells from the pseudoglandular period, decreased during development and almost disappeared in cells from the saccular stage. Interestingly, the response of epithelial cells to this growth-promoting activity declined with advancing gestational age as epithelial cells became more responsive to fibroblast-derived differentiation factor(s). Production of differentiation factor(s) by fibroblasts increased during the canalicular stage of lung development. Platelet-derived growth factor (PDGF) and low concentrations of transforming growth factor-beta (TGF-beta) stimulated epithelial cell proliferation. PDGF did not affect differentiation, whereas TGF-beta was inhibitory. Dependent on their proximity to the epithelium, two subpopulations of fibroblasts that differed in their ability to promote epithelial cell proliferation or differentiation were isolated. Fibroblasts in close proximity to the epithelium mainly produced differentiation factors, whereas more distant fibroblasts primarily stimulated proliferation.
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Fukumoto, Satoshi, Takayoshi Kiba, Bradford Hall, Noriyuki Iehara, Takashi Nakamura, Glenn Longenecker, Paul H. Krebsbach, Antonio Nanci, Ashok B. Kulkarni, and Yoshihiko Yamada. "Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts." Journal of Cell Biology 167, no. 5 (December 6, 2004): 973–83. http://dx.doi.org/10.1083/jcb.200409077.

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Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin-null mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.
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Gao, Xia, Aman S. Bali, Scott H. Randell, and Brigid L. M. Hogan. "GRHL2 coordinates regeneration of a polarized mucociliary epithelium from basal stem cells." Journal of Cell Biology 211, no. 3 (November 2, 2015): 669–82. http://dx.doi.org/10.1083/jcb.201506014.

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Pseudostratified airway epithelium of the lung is composed of polarized ciliated and secretory cells maintained by basal stem/progenitor cells. An important question is how lineage choice and differentiation are coordinated with apical–basal polarity and epithelial morphogenesis. Our previous studies indicated a key integrative role for the transcription factor Grainyhead-like 2 (Grhl2). In this study, we present further evidence for this model using conditional gene deletion during the regeneration of airway epithelium and clonal organoid culture. We also use CRISPR/Cas9 genome editing in primary human basal cells differentiating into organoids and mucociliary epithelium in vitro. Loss of Grhl2 inhibits organoid morphogenesis and the differentiation of ciliated cells and reduces the expression of both notch and ciliogenesis genes (Mcidas, Rfx2, and Myb) with distinct Grhl2 regulatory sites. The genome editing of other putative target genes reveals roles for zinc finger transcription factor Znf750 and small membrane adhesion glycoprotein in promoting ciliogenesis and barrier function as part of a network of genes coordinately regulated by Grhl2.
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Dissertations / Theses on the topic "Epithelium Cell differentiation"

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San, Roman Adrianna Katrina. "Mechanisms of Stem Cell Maintenance and Cell Differentiation in the Intestinal Epithelium." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14226057.

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Constant regeneration of the intestinal epithelium, a dynamic tissue with vital digestive and barrier functions, depends on proliferation of resident stem cells and their differentiation into mature cell types. This epithelium thus provides an ideal model to study stem cells and mechanisms of cell differentiation in an adult tissue. The identification of a proliferative population of intestinal stem cells (ISCs) at the base of intestinal crypts presents the prospect of understanding their regulation by extrinsic and intrinsic factors. Although activation of Wnt signaling in ISCs is thought to be one crucial function of the ISC niche, the cellular source of Wnt ligands is uncertain. Chapter 2 addresses this question through genetic elimination of Wnt ligand secretion in candidate niche cell populations. The data reveal that Wnts originating in any of the sources considered in the literature – the epithelium (including Paneth cells) and sub-epithelial myofibroblasts – are not required for ISC function. These data support models of highly complex cell redundancy or alternative, non-Wnt ligands. Chapter 3 investigates the cell-intrinsic contributions of an intestine-restricted transcription factor (TF), CDX2, to important ISC behaviors. Cdx2 loss in vivo perturbs ISC proliferation and differentiation, distinct from its functions in mature enterocytes. Analysis of candidate direct CDX2 target genes in ISCs suggests that CDX2 modulates Fibroblast Growth Factor signaling, thus opening new avenues of investigation. Although cells that differentiate from ISCs rely on gene expression changes mediated by TFs, loss of several individual TFs in vivo has modest effects on intestinal function. Chapter 4 characterizes the functional interactions of CDX2, which has many properties of a master regulator, with two other intestinal TFs: GATA4 and Hepatocyte Nuclear Factor 4 alpha (HNF4A). Analysis of compound mutant mouse intestines elucidated combinatorial roles for CDX2 with GATA4 in crypt cell proliferation and with HNF4A in enterocyte differentiation. Building on this foundation, Chapter 5 describes preliminary investigations into another TF, HNF1A, in intestinal gene regulation and its relationship with CDX2 in controlling cell differentiation and tissue architecture. These studies highlight the complexities of TF interactions and the functions of diverse TF complexes in controlling tissue-specific genes during cell differentiation.
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Shao, Xingguo. "Identification of a Tans-differentiation factor, Rad, a small Ras-like GTP-binding protein, in the regulation of epithelial cell differentiation in human airway epithelium /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.

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Ruiz-Torres, Sonya Jomara. "Modeling Fanconi Anemia in Squamous Epithelium using Human Induced Pluripotent Stem Cell-Derived Organoids." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1573573103136768.

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De, las Heras Rachel, and n/a. "Neuronal Differentiation: A Study Into Differential Gene Expression." Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040225.161725.

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Neuronal differentiation encompasses an elaborate developmental program which until recently was difficult to study in vitro. The advent of several cell lines able to differentiate in culture proved to be the turning point for gaining an understanding of molecular neuroscience. In particular the olfactory epithelium provides an attractive tool with which to investigate fundamental questions relating to neuronal differentiation, as it displays a unique capacity to regenerate and to retain a neurogenetic potential from its genesis and throughout adult life. The coordinated regulation of gene expression is fundamental to the control of neuronal differentiation. In order to reveal active processes at the molecular level and to dissect key components of molecular pathways, differential gene expression studies provide a foundation for the elucidation of dynamic molecular mechanisms. This thesis identified genes involved in neuronal differentiation by utilising a clonal olfactory receptor neuronal cell line (OLF442). Gene expression levels were identified using differential display and oligonucleotide array technology before and after serum deprivation. Differential display revealed two kinases whose expression levels were elevated during the differentiation of OLF442, identified as focal adhesion kinase (FAK) related non-kinase (FRNK) and mammalian ste20 like (MST)2 kinase. Furthermore, analysis of the oligonucleotide array data confirmed the expression of genes involved in altering presentation of extracellular matrix molecules, in mediating cytoskeletal rearrangements, and in ceasing the cell cycle, supporting the use of OLF442 as a model for studying differentiation. The differentiation of OLF442 results from the synchronisation of multiple transduction cascades and cellular responses as evidenced by the microarray data. A protein that can synchronise such signalling is the non-receptor protein tyrosine kinase, FAK. Thus the finding of the endogenous FAK inhibitor FRNK by differential display was intriguing as there was no difference in the expression level of FAK induced by differentiation, contrasting that of FRNK. This induced FRNK expression was derived autonomously as it was not responsive to the caspase-3 inhibitor, DEVD-CHO. This is particularly pertinent since the primary role of FRNK is to act as an inhibitor of FAK by competing with its substrates and reducing the phosphorylation of both FAK and its associated proteins. Differential display also revealed the upregulation of another kinase, which had 90% homology with rat MST2 kinase within the 3' UTR. Both mouse MST2 kinase (sequence submitted to GenBank, accession number AY058922) and the closely related family member MST1 kinase were sequenced and cloned. Moreover, evidence to support an autonomously expressed carboxyl-terminal domain of MST2 kinase is presented in Chapter 3 and provides a unique way in which MST2 may regulate its own activity. To further understand the role of MST in neuronal differentiation, a series of stable OLF442 transfections (with mutant and wild-type MST constructs) were carried out. MST was localised with cytoplasmic structures that may represent actin stress fibres, indicating a potential cytoskeletal role during neuronal differentiation. This indicated that MST1 may play a role in the morphological processes involved in neuronal differentiation. The identification of two kinases by differential display provided the motivation to understand the cellular context of OLF442 and to determine the phosphorylation status of the mitogen-activated protein kinase (MAPK) signalling cascades. Differentiation of OLF442 induced high-level phosphorylation of a putative B-Raf isoform, MEK2 and ERK1/2. Interestingly, there was a switch between preferential phosphorylation of MEK1 in undifferentiated OLF442 to preferential phosphorylation of MEK2 following differentiation. SAPK/JNK was also phosphorylated, as was the transcription factor c-Jun, which is a common substrate of both the ERK and SAPK/JNK signalling modules. The mapping of the cellular context of differentiating OLF442 has identified a promising model of a novel MAPK module. This consists of FAK signalling through Rap1 to ERK providing sustained activation, which is buffered or terminated by the expression of the endogenous FAK inhibitor FRNK. Furthermore, MST kinase could potentially play a role in regulating the cytoskeletal re-arrangements that are necessary for neuronal differentiation. MST kinase may signal transiently via the SAPK pathway to provide concomitant activation of c-Jun that is required for neuronal differentiation. An understanding of the gene expression pattern of the normal neuronal differentiation program allows a greater understanding of potential developmental aberrations. This could provide an opportunity for therapies to be conceived, while understanding the complexity of neuronal determination could also provide opportunities for stem cell transplantation.
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Alwosaibai, Kholoud. "Role of PAX2 in Maintaining the Differentiation of Oviductal Epithelium and Inhibiting the Transition to a Stem Cell State." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34450.

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Several studies have proposed the fallopian tube epithelium as a site of origin of ovarian cancer. The discovery of precursor lesions in the fallopian tube in patients at risk for ovarian cancer supports a probable origin for high-grade serous ovarian carcinoma in this tissue. While the fallopian tube epithelium consists of three distinct cell types, the paired box protein 2 (PAX2) positive cells and potentially the CD44 positive stem-like cells are most relevant to ovarian cancer. Loss of PAX2 expression in the fallopian tube cells is considered to be an early event in epithelial transformation, but the specific role of PAX2 in this transition is unknown. The aim of this study was to define the role of PAX2 in oviductal epithelial cells (OVE) cells and in mouse ovarian surface epithelial cells (MOSE), and to understand its contribution to the formation of serous precursor lesions in the fallopian tubes. Herein, we studied the OVE response to transforming growth factor β (TGFβ, a cytokine found in follicular fluid) and provide evidence of its potential involvement in the regulation of stem cell-like behaviors that may contribute to formation of cancer-initiating cells. Treatment of primary cultures of OVE cells with TGFβ at concentrations found in ovulatory follicular fluid induced an epithelial-mesenchymal transition (EMT) with expected changes in proliferation, cell morphology and expression of SNAIL, Vimentin and E-cadherin. EMT was also associated with decreased expression of PAX2 and an increase in the fraction of cells expressing CD44. Pax2 knockdown in OVE cells and overexpression in ovarian epithelial cells confirmed that PAX2 inhibits CD44 expression and regulates the degree of epithelial differentiation of OVE cells. These results suggest that the loss of PAX2 seen in serous tubal intraepithelial carcinomas (STIC) leads to a shift to a more mesenchymal phenotype associated with stem-like features. Pax2 overexpression in MOSE cells also induced the formation of vascular channels both in vitro and in vivo, which indicate a possible contribution of PAX2 to ovarian cancer progression by increasing the vascular channels to supply nutrients to the tumor cells. Furthermore, since loss of PAX2 in STIC was found associated with P53 and BRCA1 mutations, OVE cells with mutations of the tumor suppressor genes Trp53 and Brca1 were studied. We found that loss of Trp53 with or without loss of Brca1 increased cell proliferation and colony formation in vitro. In addition, loss of Trp53 induced OVE cells to undergo EMT and induced the expression of stem cell–associated genes. We therefore suggest a potential contribution of stem cells in initiating the precursor lesions in the fallopian tubes in combination with tumor suppressor gene mutation.
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Tanaka, Elly M., Yu Zhu, Madalena Carido, Andrea Meinhardt, Thomas Kurth, Mike O. Karl, and Marius Ader. "Three-Dimensional Neuroepithelial Culture from Human Embryonic Stem Cells and Its Use for Quantitative Conversion to Retinal Pigment Epithelium." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-191613.

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A goal in human embryonic stem cell (hESC) research is the faithful differentiation to given cell types such as neural lineages. During embryonic development, a basement membrane surrounds the neural plate that forms a tight, apico-basolaterally polarized epithelium before closing to form a neural tube with a single lumen. Here we show that the three-dimensional epithelial cyst culture of hESCs in Matrigel combined with neural induction results in a quantitative conversion into neuroepithelial cysts containing a single lumen. Cells attain a defined neuroepithelial identity by 5 days. The neuroepithelial cysts naturally generate retinal epithelium, in part due to IGF-1/insulin signaling. We demonstrate the utility of this epithelial culture approach by achieving a quantitative production of retinal pigment epithelial (RPE) cells from hESCs within 30 days. Direct transplantation of this RPE into a rat model of retinal degeneration without any selection or expansion of the cells results in the formation of a donor-derived RPE monolayer that rescues photoreceptor cells. The cyst method for neuroepithelial differentiation of pluripotent stem cells is not only of importance for RPE generation but will also be relevant to the production of other neuronal cell types and for reconstituting complex patterning events from three-dimensional neuroepithelia.
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Naillat, F. (Florence). "Roles of Wnt4/5a in germ cell differentiation and gonad development & ErbB4 in polarity of kidney epithelium." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514295751.

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Abstract The embryonic urogenital system generates the metanephric kidneys, the gonads and the adrenal glands, and its development is based on sequential and reciprocal cell and tissue interactions. The mechanisms which regulate urogenital ontogeny are still poorly understood. In this thesis, the roles of Wnt-4 and ErbB4 functions in gonad and kidney development were analysed by using in vivo functional genomic technologies. Wnt-4 is crucial in female development since its absence leads to a partial female to male sex reversal. We found that Wnt-4 mediated the interactions between the somatic and the germ cells and played a role in meiosis which is regulated in part by the secreted signal retinoic acid (RA). Expression of certain meiosis-controlling genes (Stra8, Spo11) was inhibited in the Wnt-4 deficient germ cells, while certain pluripotency genes (Oct4, Fgf9, Sox2 and Dnmt3l) were activated similarly as in the wild-type male gonad. In addition to this, we noted that a gene encoding for a Cyp26b1 enzyme, which degrades RA in the embryonic testis, was ectopically expressed in the Wnt-4 deficient ovary. Microarray analysis was used to identify candidate Wnt-4 target genes by using the Wnt-4 knock-out mouse. Of these genes, Runx-1 may represent a novel signalling target to mediate Wnt-4 activity in the control female development The role of receptor-tyrosine kinase ErbB4 in kidney development was studied by using both in vivo gain and loss of function approaches. In the gain-of-function situation, we found that certain markers for the epithelial tubules and collecting ducts lost their polarized expression pattern. At the same time, the orientation of the cells in the kidney tubules was deregulated and an increase in cell proliferation was noticed. We suggest that the observed defects gave rise to an increase in the tubule diameter and to cyst formation in the kidney cortex. In the loss-of-function mouse, the lack of ErbB4 expression led to a similar phenotype as with the gain of function, and the renal functions of the mutant adult kidneys were compromised. In conclusion, the results point to specific roles for Wnt-4 and ErbB4 in the control of urogenital development. Wnt-4 appears to be crucial in sustaining proper female somatic cell and germ cell differentiation, and maintenance of gonad development during and after the sex determination event, while ErbB4 activity is critical for the regulation of tubular growth in embryonic kidney development
Tiivistelmä Sekä nisäkkään jälkimunuainen, lisämunuainen että sukurauhanen kehittyvät alkion urogenitaalialueen järjestelmästä ja solu- ja kudosvuorovaikutukset ohjaavat elinkehitysprosessia. Tapahtuman molekyylitason mekanismit ovat kuitenkin huonosti tunnettuja. Tässä väitöskirjatyössä tutkittiin Wnt-4 signaalin tehtäviä sukurauhasen ja ErbB4- proteiinin munuaisen kehityksessä. Wnt-4 signaali on keskeinen naisen sukupuolisuuden kehityksessä, koska signaalin puutos aiheuttaa alkion sukupuolen osittaisen kääntymisen naaraasta koiraaksi. Tarkastelimme aluksi sitä, välittääkö Wnt-4 itusolujen ja sukurauhasen somaattisten solujen vuorovaikutuksia ohjaten itusolujen meioosia, jota mm. A-vitamiini säätelee. Havaitsimme, että Wnt-4 geeni puuttuessa tietyt meioosia säätelevät geenit kuten Stra8 ja Spo11 olivat heikentyneet, kun taas solujen monikykyisyyteen liittyvät geenit kuten Oct4, Fgf9, Sox2 ja Dnmt3l aktivoituivat vastaavalla tavalla kuin havaitaan normaalisti koirasalkion kivesaiheessa. Tämän lisäksi havaitsimme, että Cyp26b1-geeni, joka johtaa A-vitamiinin hajoamiseen alkiossa ja estää normaalisti meioosin koirasalkion kivesaiheessa oli aktivoitunut munuaisrauhasaiheessa, jolta puuttuu Wnt-4 aktiivisuus. Tuloksemme osoittavat, että Wnt-4 säätelee osaltaan naarasalkion itusolujen meioosia. Tarkastelimme myös mikrosirututkimusten avulla niitä geenejä, joita Wnt-4 säätelee sukuelinaiheessa. Identifioimme useissa Wnt ja β-catenin signaalireittiin liittyvissä geeneissa muutoksia. Muuntuneet geenit voivat olla Wnt-4 signaalireitin kohdegeenejä. Näistä Runx-1 saattaa olla keskeinen Wnt signaalitien kohdegeeni, joka säätelee merkittävällä tavalla naaraan munarauhasen kehitystä. Väitöskirjan toisessa osassa tarkastelimme ErbB4-reseptorityrosiinikinaasin tehtäviä munuaisen kehityksen säätelyssä. ErbB4-geenin tehtäviä tutkittiin käyttäen hyväksi siirtogeenisiä malliorganismeja, joissa ErbB4-geenin määrä oli joko koholla tai ajastetusti inaktivoitu. ErbB4- geenin kokeellinen yliaktiivisuus muutti spesifisti tekijöitä, jotka säätelevät osaltaan jälkimunuaisen epiteeliputkien solujen orientaatiota ja solun jakautumista. Solujen orientaatiomuutoksen yhteydessä myös solujen jakautuminen häiriintyi. Oletuksemme on, että nämä epiteelikudoksessa tapahtuneet muutokset ovat syy, miksi kohotettu ErbB4-aktiviteetti muuttaa epiteeliputkien paksuutta ja pituutta erityisesti munuaisen pintakerroksissa. Havaitsimme myös, että ErbB4-geenin ajastettu poistaminen munuaisen epiteelikudoksessa johti hyvin samankaltaisiin, mutta vastakkaisiin muutoksiin kuin ErbB4-aktiviteetin kohottaminen. Muutokset johtivat myös muutoksiin munuaisen toiminnassa. Yhteenvetona toteamme, että näillä Wnt-4 ja ErbB4 solusignallointiin liittyvillä molekyyleillä on keskeinen tehtävä alkion munarauhasen ja munuaisen aiheen kehityksen säätelyssä. Wnt-4 ohjaa sekä itusolujen että somaattisten solujen erilaistumista ja samalla sukupuolen määräytymistä ja jatkokehitystä, kun taas ErbB4-signallointireseptorin tehtävä on avainasemassa munuaisen epiteeliputken kasvun säätelyssä
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Tanaka, Elly M., Yu Zhu, Madalena Carido, Andrea Meinhardt, Thomas Kurth, Mike O. Karl, and Marius Ader. "Three-Dimensional Neuroepithelial Culture from Human Embryonic Stem Cells and Its Use for Quantitative Conversion to Retinal Pigment Epithelium." Public Library of Science, 2013. https://tud.qucosa.de/id/qucosa%3A29136.

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A goal in human embryonic stem cell (hESC) research is the faithful differentiation to given cell types such as neural lineages. During embryonic development, a basement membrane surrounds the neural plate that forms a tight, apico-basolaterally polarized epithelium before closing to form a neural tube with a single lumen. Here we show that the three-dimensional epithelial cyst culture of hESCs in Matrigel combined with neural induction results in a quantitative conversion into neuroepithelial cysts containing a single lumen. Cells attain a defined neuroepithelial identity by 5 days. The neuroepithelial cysts naturally generate retinal epithelium, in part due to IGF-1/insulin signaling. We demonstrate the utility of this epithelial culture approach by achieving a quantitative production of retinal pigment epithelial (RPE) cells from hESCs within 30 days. Direct transplantation of this RPE into a rat model of retinal degeneration without any selection or expansion of the cells results in the formation of a donor-derived RPE monolayer that rescues photoreceptor cells. The cyst method for neuroepithelial differentiation of pluripotent stem cells is not only of importance for RPE generation but will also be relevant to the production of other neuronal cell types and for reconstituting complex patterning events from three-dimensional neuroepithelia.
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Vasconcelos, Michelle. "O papel da sinalização Notch na diferenciação do epitélio pulmonar." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-16052012-100050/.

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O epitélio pulmonar é formado por uma grande diversidade celular, que incluí: células secretoras, ciliadas, basais e neuroendócrinas (NE). A distribuição balanceada destes tipos celulares é crucial para a função pulmonar e pode ser dramaticamente alterada em doenças como a asma. Neste trabalho, estudamos o papel de Notch no pulmão em desenvolvimento ao inativar condicionalmente Rbpjk ou Pofut1, componentes críticos da sinalização Notch. Pulmões mutantes apresentaram-se superpopulados por células ciliadas e NE, além da ausência de células de Clara. Nossos dados sugeriram que Notch suprime os programas de diferenciação de células ciliadas e NE para permitir a diferenciação de células de Clara, através de um mecanismo de inibição lateral. Identificamos também genes associados com a diferenciação de células secretoras e ciliadas através de microarrays. A heterogeneidade no padrão de expressão gênica sugeriu que a via de sinalização Notch estabelece múltiplos subtipos de células ciliadas e secretoras no epitélio pulmonar em desenvolvimento.
The airway epithelium comprises a diverse population of secretory, ciliated, basal and neuroendocrine cells (NE). The proper balance of these cell types is critical for normal lung function and can be altered dramatically in conditions, such as asthma. We studied the role of Notch in airway progenitor cell fate by conditionally inactivating Rbpjk or Pofut1, two critical Notch pathway components in mouse mutants. This resulted in airways overpopulated with ciliated and NE cells and absence of secretory Clara cells. We found that Notch suppresses the ciliated and the NE cell programs to allow secretory cell differentiation through a lateral inhibition mechanism. We also identified genes associated with the differentiation of secretory and ciliated cells through a microarray gene profiling experiment. The great heterogeneity of gene expression patterns suggested that Notch plays a role in establishing multiple subsets of secretory and ciliated cells in the developing lung.
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Zhao, Haotian. "Exploring the role of fibroblast growth factor (FGF) signaling in mouse lens fiber differentiation through tissue-specific disruption of FGF receptor gene family." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1072722841.

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Thesis (Ph. D.)--Ohio State University, 2004.
Title from first page of PDF file. Document formatted into pages; contains xii, 203 p.; also includes graphics (some col.) Includes bibliographical references (p. 179-203). Available online via OhioLINK's ETD Center
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Books on the topic "Epithelium Cell differentiation"

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Kaur, Maninder. Growth and differentiation of liver epithelial cells. Birmingham: University of Birmingham, 2001.

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Beaulieu, Jean-François. Extracellular matrix components and integrins in relationship to human intestinal epithelial cell differentiation. Stuttgart: G. Fischer, 1997.

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Tissue remodeling and epithelial morphogenesis. San Diego: Elsevier/Academic Press, 2009.

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Pierre, Savagner, ed. Rise and fall of epithelial phenotype: Concepts of epithelial-mesenchymal transition. Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2005.

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Savagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition (Molecular Biology Intelligence Unit). Springer, 2005.

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Savagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition. Springer, 2010.

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1943-, McDonald John A., ed. Lung growth and development. New York: M. Dekker, 1997.

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United States. National Aeronautics and Space Administration., ed. Morphological differentiation of colon carcinoma cell lines in rotating wall vessels. [Washington, DC: National Aeronautics and Space Administration, 1994.

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Morioka, K. Hair Follicle: Differentiation under the Electron Microscope - An Atlas. Springer, 2004.

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Morioka, K. Hair Follicle: Differentiation under the Electron Microscope - An Atlas. Springer, 2010.

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Book chapters on the topic "Epithelium Cell differentiation"

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Breunig, Esther, Dirk Czesnik, Fabiana Piscitelli, Vincenzo Di Marzo, Ivan Manzini, and Detlev Schild. "Endocannabinoid Modulation in the Olfactory Epithelium." In Results and Problems in Cell Differentiation, 139–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14426-4_11.

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Marikawa, Yusuke, and Vernadeth B. Alarcon. "Creation of Trophectoderm, the First Epithelium, in Mouse Preimplantation Development." In Results and Problems in Cell Differentiation, 165–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-30406-4_9.

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Hahn, Ursula, D. Schuppan, E. G. Hahn, H. J. Merker, and E. O. Riecken. "Cell-Matrix Interaction in the Differentiation of the Intestinal Epithelium." In Mesenchymal-Epithelial Interactions in Neural Development, 111–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71837-3_9.

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Ballios, Brian G., Valeria Marigo, and Derek van der Kooy. "Directed Differentiation of Photoreceptors and Retinal Pigment Epithelium from Adult Mouse Retinal Stem Cells." In Neural Stem Cell Assays, 129–35. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118308295.ch14.

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Riechmann, Veit. "In vivo RNAi in the Drosophila Follicular Epithelium: Analysis of Stem Cell Maintenance, Proliferation, and Differentiation." In Methods in Molecular Biology, 185–206. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7108-4_14.

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Quaranta, Vito. "Integrin Expression and Epithelial Cell Differentiation." In Cell Adhesion Molecules, 13–27. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2830-2_2.

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Yeh, Yi-Chun, and Ming-Jer Tang. "Functions of DDR1 in Epithelial Cell Differentiation." In Discoidin Domain Receptors in Health and Disease, 239–58. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6383-6_13.

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Lever, Julia E. "Inducers of Dome Formation in Epithelial Cell Cultures including Agents That Cause Differentiation." In Tissue Culture of Epithelial Cells, 3–22. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_1.

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Kamalati, Tahereh, Birunthi Niranjan, Amanda Atherton, Ramasawamy Anbazhaghan, and Barry Gusterson. "Differentiation antigens in stromal and epithelial cells of the breast." In Mammary Tumor Cell Cycle, Differentiation, and Metastasis, 227–42. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1259-8_12.

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Mort, Richard L., Panagiotis Douvaras, Steven D. Morley, Natalie Dorà, Robert E. Hill, J. Martin Collinson, and John D. West. "Stem Cells and Corneal Epithelial Maintenance: Insights from the Mouse and Other Animal Models." In Results and Problems in Cell Differentiation, 357–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-30406-4_19.

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Conference papers on the topic "Epithelium Cell differentiation"

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Didon, Lukas, Ion Wa Chao, Jasen P. Murray, David T. Dang, Rachel K. Zwick, Neil R. Hackett, and Ronald G. Crystal. "Basal Cell Differentiation Toward The Foxj1-induced Ciliated Cell Lineage In The Human Airway Epithelium." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3753.

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Koppes, Ryan A., Andrew K. Mason, Sarah B. Peters, Shayoni Ray, Melinda Larsen, and David T. Corr. "The Viscoelastic Properties of Mouse Embryonic Salivary Glands." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14600.

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Normal organ development, function, and repair are coordinated by interactions between the epithelium and the surrounding stromal cell populations. Cellular function and homeostasis are controlled by an array of chemical and physical cues originating from the cells themselves and from the surrounding extracellular matrix (ECM). Both the endogenous cell population and ECM modulate and rely on the maintenance of basal level of tension within the tissue as a cue for growth and differentiation [1]. Furthermore, the loss of this tensional homeostasis is synonymous with many pathological conditions including; cancer, wound healing, and degenerative diseases [2].
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Xiong, Zhaohui, Shuang Ren, Hao Chen, Yao Liu, Caizhi Huang, Yawan Lyvia Zhang, Joab Otieno Odera, et al. "Abstract 4471: Pax9 regulates squamous cell differentiation and alcohol-associated carcinogenesis in the oro-esophageal epithelium." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4471.

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LeBlanc, M., M. Rostami, W. L. Zuo, J. G. Mezey, M. J. Thomas, J. Schymeinsky, K. Quast, S. Visvanathan, J. S. Fine, and R. G. Crystal. "Smoking-Induced Heterogeneity and Altered Differentiation Pathways of the Progenitor Cell Population of the Human Small Airway Epithelium." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4053.

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Xu, Zhibo B., Ann E. Tilley, Jacqueline Salit, and Ronald G. Crystal. "SPDEF, A Transcription Factor Regulator Of Goblet Cell Differentiation, Is Up-regulated By Smoking In Human Small Airway Epithelium." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6760.

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Rostami, M. R., M. G. LeBlanc, W. L. Zuo, P. L. Leopold, and R. G. Crystal. "Smoking and Lung Defense: Single Cell Transcriptome Analysis of Human Small Airway Epithelium Demonstrates Smoking-Suppression of Club Cell Differentiation to a Defense Effector Role." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6397.

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Montgomery, M. T., C. M. Moore, J. L. Everman, C. Rios, K. C. Goldfarbmuren, D. Lafkas, and M. A. Seibold. "Single Cell RNA-seq Characterization of SPDEF Knock-Out in the Mucociliary Epithelium Reveals Mechanisms of Mucus Cell Differentiation in Both the Healthy and Inflamed Airways." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6147.

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Holfinger, Steven, Rashmeet Reen, William Ackerman, Douglas Kniss, and Keith J. Gooch. "PANC-1 Migration and Cluster Formation is Regulated by Short Range Mechanical Forces." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53593.

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Islet cell transplantation has already shown improved control of glucose levels and the potential to achieve insulin independence in type 1 diabetes mellitus, however there is a shortage of organ donors needed to match patient needs [1–2]. In the search for alternative sources of islets, many cell types have shown signs of β-cell differentiation by secreting c-peptide, insulin, and glucagon [3–5]. When maintained in serum-free medium, human epithelial-like pancreatic adenocarcinoma (PANC-1) cells and human-islet derived precursor cells (hIPCs) can go through a morphological transition and cluster [6]. These islet-like cell aggregates subsequently express glucagon, somatostatin, and insulin, indicating that clustering may play an important role in differentiation towards β-cells [7].
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Leahy, Rachel, Weiling Xu, Suzy A. A. Comhair, and Serpil C. Erzurum. "Hypoxia In Airway Epithelial Cell Differentiation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5115.

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Wallin, R., and S. R. Rannels. "IDENTIFICATION OF VITAMIN K-DEPENDENT CARBOXYLASE ACTIVITY AND EVIDENCE FOR PROTHROMBIN SYNTHESIS IN ALVEOLAR TYPE II CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644318.

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Prothrombin precursors have been shown to be present in micro-somes from lung alveolar type II cells. Immunoblotting revealed two microsomal precursors of apparent mol. wt. 68 and 65 kDa. The 65 kDa protein appears to be the substrate for the vitamin Independent carboxylase. Fluorography of [14c]-labeled precursors of vitamin K-dependent proteins in lung microsomes shows that the lung has several precursors that are not found in the liver. Pulmonary macrophages appear to be devoid of vitamin K-dependent carboxylase activity. However, type II epithelial cells have significant activity and this activity was unaltered when these cells were maintained in primary culture for 3 days, suggesting that carboxylase activity is expressed in alveolar epithelium independent of culture-induced changes in cellular differentiation. Carboxylase activity in type II cells was enhanced 2-fold when cells were cultured for 24 hours in the presence of 50 μM warfarin. Type II cells, therefore, resemble hepatocytes with regard to their response to coumarin drugs. Our data suggest that macrophages and type II cells may act in a cooperative manner to contribute to extravascular coagulation in the lung. Supported by NIH Grant HL-32070-02 and by The American Heart Association.
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Reports on the topic "Epithelium Cell differentiation"

1

Furuta, Saori. Roles of Breast Cancer Susceptibility Genes BRCA's in Mammary Epithelial Cell Differentiation. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada462337.

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Furuta, Saori. Roles of Breast Cancer Susceptibility Genes BRCA's in Mammary Epithelial Cell Differentiation. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada469943.

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Pauley, Robert J. Determinants of Human Breast Epithelial Cell Estrogen Expression and Differentiation: Organization and Environment. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada374045.

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Setaluri, Vijayasaradhi. Differentiation of Neonatal Human-Induced Pluripotent Stem Cells to Prostate Epithelial Cells: A Model to Study Prostate Cancer Development. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada583418.

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Setaluri, Vijayasaradhi. Differentiation of Neonatal Human-Induced Pluripotent Stem Cells to Prostate Epithelial Cells: A Model to Study Prostate Cancer Development. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada609443.

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Guo, Xuning E. Pilot Study on Factors Secreted by Differentiating Mammary Epithelial Cells (MECs) That Can Suppress Proliferation of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada492688.

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