scholarly journals Alk5-Mediated Transforming Growth Factor   Signaling Acts Upstream of Fibroblast Growth Factor 10 To Regulate the Proliferation and Maintenance of Dental Epithelial Stem Cells

2011 ◽  
Vol 31 (10) ◽  
pp. 2079-2089 ◽  
Author(s):  
H. Zhao ◽  
S. Li ◽  
D. Han ◽  
V. Kaartinen ◽  
Y. Chai
Keyword(s):  
Stem Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Transforming Growth Factor ◽  
Growth Factor Signaling ◽  
Fibroblast Growth ◽  
Epithelial Stem Cells ◽  
Fibroblast Growth Factor 10

scholarly journals Fibroblast Growth Factor Signaling Is Essential for Self-renewal of Dental Epithelial Stem Cells

2013 ◽  
Vol 288 (40) ◽  
pp. 28952-28961 ◽  
Author(s):  
Julia Yu Fong Chang ◽  
Cong Wang ◽  
Junchen Liu ◽  
Yanqing Huang ◽  
Chengliu Jin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Growth Factor Signaling ◽  
Fibroblast Growth ◽  
Epithelial Stem Cells ◽  
Fibroblast Growth Factor Signaling ◽  
Self Renewal

scholarly journals Fibroblast growth factor receptor-3 regulates Paneth cell lineage allocation and accrual of epithelial stem cells during murine intestinal development

2009 ◽  
Vol 297 (1) ◽  
pp. G168-G178 ◽  
Author(s):  
Alda Vidrich ◽  
Jenny M. Buzan ◽  
Brooks Brodrick ◽  
Chibuzo Ilo ◽  
Leigh Bradley ◽  
...  
Keyword(s):  
Stem Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Paneth Cell ◽  
Cell Lineage ◽  
Growth Factor Receptor ◽  
Intestinal Development ◽  
Fibroblast Growth ◽  
Epithelial Stem Cells

Fibroblast growth factor receptor 3 (FGFR-3) is expressed in the lower crypt epithelium, where stem cells of the intestine reside. The role of FGFR-3 signaling in regulating features of intestinal morphogenesis was examined in FGFR-3-null (FGFR-3−/−) mice. FGFR-3−/− mice had only about half the number of intestinal crypts and a marked decrease in the number of functional clonogenic stem cells, as assessed by an in vivo microcolony-forming assay, compared with wild-type littermates. A marked deficit in allocation of progenitor cells to Paneth cell differentiation was noted, although all the principal epithelial lineages were represented in FGFR-3−/− mice. The total cellular content and nuclear localization of β-catenin protein were reduced in FGFR-3−/− mice, as was expression of cyclin D1 and matrix metalloproteinase-7, major downstream targets of β-catenin/T cell factor-4 (Tcf-4) signaling. Activation of FGFR-3 in Caco-2 cells, an intestinal epithelial cell line, abrogated the fall in β-catenin/Tcf-4 signaling activity that is normally observed in these cells as cultures become progressively more confluent. These findings are consistent with the hypothesis that, during intestinal development, FGFR-3 signaling regulates crypt epithelial stem cell expansion and crypt morphogenesis, as well as Paneth cell lineage specification, through β-catenin/Tcf-4-dependent and -independent pathways.

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