Nephronectin expression is regulated by SMAD signaling in osteoblast-like MC3T3-E1 cells

被引：11

作者：

Tsukasaki, Masayuki ^{[1
]}

Yamada, Atsushi ^{[1
]}

Yoshimura, Kentaro ^{[1
]}

Miyazono, Agasa ^{[2
]}

Yamamoto, Matsuo ^{[2
]}

Takami, Masamichi ^{[1
]}

Miyamoto, Yoichi ^{[1
]}

Morimura, Naoko ^{[3
]}

Kamijo, Ryutaro ^{[1
]}

机构：

[1] Showa Univ, Sch Dent, Dept Biochem, Tokyo 142, Japan

[2] Showa Univ, Sch Dent, Dept Periodontol, Tokyo 142, Japan

[3] RIKEN Brain Sci Inst, Lab Comparat Neurogenesis, Saitama, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 425卷 / 02期

基金：

日本学术振兴会;

关键词：

Nephronectin; Alk5; SMAD; TGF-BETA; BONE-FORMATION; DIFFERENTIATION; IDENTIFICATION; MEMBRANE; INTEGRIN; NUCLEUS; POEM;

D O I：

10.1016/j.bbrc.2012.07.106

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Nephronectin (Npnt) is an extracellular matrix protein known to be a ligand for the integrin alpha 8 beta 1. We previously demonstrated that Npnt expression was suppressed by TGF-beta through ERK1/2 and JNK in osteoblasts. In this study, we found that inhibition of a TGF-beta type I receptor (TGF-beta R1, Alk5) by a specific inhibitor {2-[3-(6-Methylpyridin-2-yl)-1H-pyrazol-4-yl]-1,5-naphthyridine} strongly induced Npnt expression in osteoblast-like MC3T3-E1 cells. The Alk5 inhibitor-induced increase of Npnt expression occurred in both time- and dose-dependent manners, while that expression was also induced by introduction of an siRNA for Smad2, a central intracellular mediator of TGF-beta, signaling. These results suggest that the expression of Npnt is regulated by the Alk5-SMAD signaling pathway in osteoblasts. (c) 2012 Elsevier Inc. All rights reserved.

引用

页码：390 / 392

页数：3

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