Notch signalling is required for the survival of epithelial stem cells in the continuously growing mouse incisor

2010 ◽  
Vol 80 (4-5) ◽  
pp. 241-248 ◽  
Author(s):  
Szabolcs Felszeghy ◽  
Marika Suomalainen ◽  
Irma Thesleff
2013 ◽  
Vol 19 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Miquella G. Chavez ◽  
Wenli Yu ◽  
Brian Biehs ◽  
Hidemitsu Harada ◽  
Malcolm L. Snead ◽  
...  

1999 ◽  
Vol 147 (1) ◽  
pp. 105-120 ◽  
Author(s):  
Hidemitsu Harada ◽  
Päivi Kettunen ◽  
Han-Sung Jung ◽  
Tuija Mustonen ◽  
Y. Alan Wang ◽  
...  

The continuously growing mouse incisor is an excellent model to analyze the mechanisms for stem cell lineage. We designed an organ culture method for the apical end of the incisor and analyzed the epithelial cell lineage by 5-bromo-2′-deoxyuridine and DiI labeling. Our results indicate that stem cells reside in the cervical loop epithelium consisting of a central core of stellate reticulum cells surrounded by a layer of basal epithelial cells, and that they give rise to transit-amplifying progeny differentiating into enamel forming ameloblasts. We identified slowly dividing cells among the Notch1-expressing stellate reticulum cells in specific locations near the basal epithelial cells expressing lunatic fringe, a secretory molecule modulating Notch signaling. It is known from tissue recombination studies that in the mouse incisor the mesenchyme regulates the continuous growth of epithelium. Expression of Fgf-3 and Fgf-10 were restricted to the mesenchyme underlying the basal epithelial cells and the transit-amplifying cells expressing their receptors Fgfr1b and Fgfr2b. When FGF-10 protein was applied with beads on the cultured cervical loop epithelium it stimulated cell proliferation as well as expression of lunatic fringe. We present a model in which FGF signaling from the mesenchyme regulates the Notch pathway in dental epithelial stem cells via stimulation of lunatic fringe expression and, thereby, has a central role in coupling the mitogenesis and fate decision of stem cells.


Author(s):  
Miquella G. Chavez ◽  
Jimmy Hu ◽  
Kerstin Seidel ◽  
Chunying Li ◽  
Andrew Jheon ◽  
...  

2015 ◽  
Vol 6 ◽  
Author(s):  
Giovanna Orsini ◽  
Lucia Jimenez-Rojo ◽  
Despoina Natsiou ◽  
Angelo Putignano ◽  
Thimios A. Mitsiadis

2012 ◽  
Vol 366 (2) ◽  
pp. 357-366 ◽  
Author(s):  
Chun-Ying Li ◽  
Wanghee Cha ◽  
Hans-Ulrich Luder ◽  
Roch-Philippe Charles ◽  
Martin McMahon ◽  
...  

2017 ◽  
Author(s):  
Mohit S. Verma ◽  
Michael J. Fink ◽  
Gabriel L Salmon ◽  
Nadine Fornelos ◽  
Takahiro E. Ohara ◽  
...  

Two biological activities of butyrate in the colon (suppression of proliferation of colonic epithelial stem cells and inflammation) correlate with inhibition of histone deacetylases. Cellular and biochemical studies of molecules similar in structure to butyrate, but different in molecular details (functional groups, chain-length, deuteration, oxidation level, fluorination, or degree of unsaturation) demonstrated that these activities were sensitive to molecular structure, and were compatible with the hypothesis that butyrate acts by binding to the Zn<sup>2+</sup> in the catalytic site of histone deacetylases. Structure-activity relationships drawn from a set of 36 compounds offer a starting point for the design of new compounds targeting the inhibition of histone deacetylases. The observation that butyrate was more potent than other short-chain fatty acids is compatible with the hypothesis that crypts evolved (at least in part), to separate stem cells at the base of crypts from butyrate produced by commensal bacteria.


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