Stress to endoplasmic reticulum of mouse osteoblasts induces apoptosis and transcriptional activation for bone remodeling

被引：80

作者：

Hamamura, Kazunori ^{[1
]}

Yokota, Hiroki ^{[1
]}

机构：

[1] Indiana Univ Purdue Univ, Dept Biomed Engn & Anat & Cell Biol, Indianapolis, IN 46202 USA

来源：

FEBS LETTERS | 2007年 / 581卷 / 09期

关键词：

Osteoblasts; ER stress; ATF4; apoptosis; bone remodeling;

D O I：

10.1016/j.febslet.2007.03.063

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：

ATF4 is an essential regulator in osteogenesis as well as in stress responses to the endoplasmic reticulum (ER). We addressed a question: Does ER stress to osteoblasts upregulate ATF4 expression? If so, do they exhibit ATF4-mediated bone remodeling or apoptosis? ER stress, induced by Thapsigargin and tunicamycin, elevated a phosphorylated form of eIF2 alpha and ATF4, but the cellular fate depended on treatment duration. The treatment for 1 h, for instance, activated Runx2, and type I collagen, while the treatment for 24 h induced apoptosis. Our observations suggest that there is a threshold for ER stress and osteoblasts present a bi-phasic pattern of their fate. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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收藏

页码：1769 / 1774

页数：6

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