scholarly journals Role of stromal tenascin-C in mouse prostatic development and epithelial cell differentiation

2008 ◽  
Vol 324 (2) ◽  
pp. 310-319 ◽  
Author(s):  
Kenichiro Ishii ◽  
Kyoko Imanaka-Yoshida ◽  
Toshimichi Yoshida ◽  
Yoshiki Sugimura
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Tenascin C ◽  
Epithelial Cell Differentiation

STROMAL TENASCIN-C SIGNAL REGULATES MOUSE PROSTATIC DEVELOPMENT AND EPITHELIAL CELL DIFFERENTIATION

2009 ◽  
Vol 181 (4S) ◽  
pp. 395-395
Author(s):  
Kenichiro Ishii ◽  
Kyoko Imanaka-Yoshida ◽  
Tetsuya Imamura ◽  
Shigeki Arase ◽  
Yuko Yoshio ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Tenascin C ◽  
Epithelial Cell Differentiation

Multifaceted role of keratins in epithelial cell differentiation and transformation

2019 ◽  
Vol 44 (2) ◽  
Author(s):  
Crismita Dmello ◽  
Saumya S Srivastava ◽  
Richa Tiwari ◽  
Pratik R Chaudhari ◽  
Sharada Sawant ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Epithelial Cell Differentiation

scholarly journals Ancestral role of TNF-R pathway in cell differentiation in the basal metazoan Hydra

2020 ◽  
pp. jcs.255422
Author(s):  
Mona Steichele ◽  
Lara S. Sauermann ◽  
Ann-Christine König ◽  
Stefanie Hauck ◽  
Angelika Böttger
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Tumour Necrosis ◽  
Apoptotic Pathway ◽  
Epithelial Cell Differentiation ◽  
Basal Metazoan ◽  
Mediate Cell ◽  
Death Effector ◽  
Body Column

Tumour necrosis factor receptors (TNF-Rs) and their ligands, tumour necrosis factors are highly conserved proteins described in all metazoan phyla. They function as inducers of extrinsic apoptotic signalling and facilitate inflammation, differentiation and cell survival. TNF-Rs use distinct adaptor molecules to activate signalling cascades. FADD-adaptors often mediate apoptosis and TRAF-adaptors mediate cell differentiation and inflammation. Most of these pathway components are conserved in cnidarians and here we investigated the Hydra TNF-R. We report that it is related to the ectodysplasin receptor, which is involved in epithelial cell differentiation in mammals. In Hydra, it is localised in epithelial cells with incorporated nematocytes in tentacles and body column, indicating a similar function. Further experiments suggest that it interacts with the Hydra homolog of a TRAF-adaptor, but not with FADDs. Hydra-FADD proteins co-localised with Hydra caspases in death effector filaments and recruited caspases suggesting that they are part of an apoptotic signalling pathway. Regulating epithelial cell differentiation via TRAF-adaptors therefore seems to be an ancient function of TNF-Rs, whereas FADD-caspase interactions may be part of a separate apoptotic pathway.

scholarly journals The Role of Fgf Signaling on Epithelial Cell Differentiation in Mouse Vagina

In Vivo ◽  
2019 ◽  
Vol 33 (5) ◽  
pp. 1499-1505
Author(s):  
YU HIRANO ◽  
KENTARO SUZUKI ◽  
TAISEN IGUCHI ◽  
GEN YAMADA ◽  
SHINICHI MIYAGAWA
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Fgf Signaling ◽  
Epithelial Cell Differentiation

Mammary epithelial cell differentiation in vitro is regulated by an interplay of EGF action and tenascin-C downregulation

1995 ◽  
Vol 108 (6) ◽  
pp. 2445-2456 ◽  
Author(s):  
G. Wirl ◽  
M. Hermann ◽  
P. Ekblom ◽  
R. Fassler
Keyword(s):  
Mammary Gland ◽  
Cell Differentiation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
Potent Inducer ◽  
Tenascin C ◽  
Epithelial Cell Differentiation

Expression of the extracellular matrix glycoprotein tenascin-C in the mammary gland is associated with cellular proliferation and cell motility during organogenesis and tumorigenesis. Because the source and the regulation of tenascin-C in these tissues are unclear, we have used tenascin-C cDNA, FITC-immunofluorescence and immuno-precipitation to examine tenascin-C expression of mammary epithelial cells. Using several mammary epithelial cell lines we could show that tenascin-C can be produced and secreted by epithelial cells. However it was found that tenascin-C synthesis was inversely correlated with the polarized epithelial phenotype. Among three mouse mammary epithelial cell clones, tenascin-C expression was most abundant in HC-11 cells, the least differentiated cell type. Expression levels were high during the growth phase but were nearly abolished when cells were grown to confluence and induced to express milk proteins. Downregulation of tenascin-C by EGF apparently commits HC-11 cells to respond to lactogenic hormones and consequently, hormone induced levels of beta-casein mRNA decreased significantly when HC-11 cells were grown on a tenascin-C substrate. On the other hand, TGF-beta, another growth factor involved in coordinated growth and differentiation of the mammary gland in vivo was found to be a very potent inducer of tenascin-C. The generation of fully polarized and tight epithelium affected the levels of tenascin-C expression. In contrast to HC-11 cells, which do not form epithelial domes in vitro, highly polarized and dome forming EpH4 and Fos-ER cells nearly lacked tenascin-C. Similarly, induction of dome formation in the rat mammary stem cell line Rama 25 by the differentiation inducer dimethylsulfoxide caused a loss of TN-C-transcripts. The inability of Fos-ER cells to develop domes in the presence of soluble tenascin-C also suggests its interference with induction and maintenance of mammary epithelial cell differentiation.

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