TGF-β signaling plays an essential role in the growth and maintenance of intervertebral disc tissue

被引：90
作者：
Jin, Hongting [2 ]
Shen, Jie
Wang, Baoli [3 ,4 ]
Wang, Meina
Shu, Bing
Chen, Di [1 ]
机构：
[1] Univ Rochester, Sch Med, Ctr Musculoskeletal Res, Dept Orthopaed & Rehabil, Rochester, NY 14642 USA
[2] Zhejiang Chinese Med Univ, Inst Orthopaed & Traumatol, Hangzhou, Zhejiang, Peoples R China
[3] Tianjin Med Univ, Endocrine Res Inst, Tianjin, Peoples R China
[4] Tianjin Med Univ, Hosp Metab Dis, Tianjin, Peoples R China
来源：
FEBS LETTERS | 2011年 / 585卷 / 08期
基金：
浙江省自然科学基金;
关键词：
TGF-beta; Col2a1-CreER(T2); Intervertebral disc; Conditional knockout; MMP-13; TARGETED DISRUPTION; NUCLEUS PULPOSUS; II RECEPTOR; MOUSE; CELLS; MICE; CHONDROCYTES; DIFFERENTIATION; EXPRESSION; GENERATION;
D O I：
10.1016/j.febslet.2011.03.034
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：
TGF-beta signaling plays a critical role in cartilage and spine tissue development at embryonic stage but its role in postnatal intervertebral disc (IVD) tissue growth and maintenance remain poorly understood. In the present studies, we have deleted the Tgfbr2 gene in inner annulus fibrosus cells of the disc tissue and surrounding growth plate chondrocytes using Col2a1-CreER(T2) transgenic mice. We found that TGF-beta signaling is required for normal growth plate cartilage and endplate cartilage growth at postnatal stage. The expression of Mmp13 gene is significantly up-regulated in primary disc cells of Tgfbr2 conditional knockout mice. Deletion of the Mmp13 gene under Tgfbr2 null background completely reverses the abnormal disc phenotype found in Tgfbr2 knockout mice. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码：1209 / 1215
页数：7
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