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Smad3 contributes to positioning of proliferating cells in colonic crypts by inducing EphB receptor protein expression.

Abstract：

:Deficiency of Smad3, an intracellular mediator of TGF-β, was shown to significantly accelerate re-epithelialization of the colonic mucosa. This study was performed to investigate the molecular mechanisms by which Smad3 controls colonic epithelial cell proliferation and crypt formation. Smad3(ex8/ex8) C57BL/6 mice were used in this study and wild-type littermates served as controls. The number of proliferating cells in the isolated colonic epithelium of Smad3(-/-) mice was significantly increased compared to that in wild-type littermates. Protein levels of the cell cycle inhibitors p21 and p27 were significantly decreased, while that of c-Myc was increased in the isolated colonic epithelium from Smad3(-/-) mice. In the colonic tissue of wild-type mice, cell proliferation was restricted to the bottom of the crypts in accordance with nuclear β-catenin staining, whereas proliferating cells were located throughout the crypts in Smad3(-/-) mice in accordance with nuclear β-catenin staining, suggesting that Smad3 is essential for locating proliferating cells at the bottom of the colonic crypts. Notably, in Smad3(-/-) mice, there was loss of EphB2 and EphB3 receptor protein expression, critical regulators of proliferating cell positioning, while EphB receptor protein expression was confirmed at the bottom of the colonic crypts in wild-type mice. These observations indicated that disturbance of the EphB/ephrin B system brings about mispositioning of proliferating cells in the colonic crypts of Smad3(-/-) mice. In conclusion, Smad3 is essential for controlling number and positioning of proliferating cells in the colonic crypts and contributes to formation of a "proliferative zone" at the bottom of colonic crypts in the normal colon.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Furukawa K,Sato T,Katsuno T,Nakagawa T,Noguchi Y,Tokumasa A,Yokote K,Yokosuka O,Saito Y

doi

10.1016/j.bbrc.2011.01.045

subject

Has Abstract

pub_date

2011-02-25 00:00:00

pages

521-6

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(11)00064-7

journal_volume

405

pub_type

杂志文章

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