蛋白酪氨酸磷酸酶SHP1通过直接影响间充质干细胞分化调控骨质形成及机制  

SHP1 Regulates Bone Mass by Directing Mesenchymal Stem Cell Differentiation

作　　者：Menghui Jiang Chunxing Zheng Peishun Shou Na Li Gang Cao Qing Chen Chunliang Xu Liming Du Qian Yang Jianchang Cao Yanyan Han Fengying Li Wei Cao Feng Liu Arnold B.Rabson Arthur I.Roberts Weifen Xie 王莹 时玉舫[2,3,4] 

机构地区：[1]不详 [2]中国科学院上海生命科学研究院健康科学研究所 [3]中国科学院/上海交通大学健康科学研究所 [4]苏州大学转化医学研究院

出　　处：《科学新闻》2017年第4期148-148,共1页Science News

基　　金：科技部;国家自然科学基金委;中国科学院;上海市科委的相关资助

摘　　要：间充质干细胞（MSCs）是脂肪细胞和成骨细胞的共同源泉，其向脂肪细胞和成骨细胞分化的状态失衡与多种代谢疾病如肥胖、骨质疏松和骨硬化症等密切相关。Osteoblasts and adipocytes are derived from a common precursor, mesenchymal stem cells (MSCs). Alterations in the normal fate of differentiating MSCs are involved in the development of obesity and osteoporosis. Here, we report that viable motheaten (me(v)) mice, which are deficient in the SH2-domain-containing phosphatase-1 (SHP1), develop osteoporosis spontaneously. Consistently, MSCs from me(v)/me(v) mice exhibit significantly reduced osteogenic potential and greatly increased adipogenic potential. When MSCs were transplanted into nude mice, SHP1-deficient MSCs resulted in diminished bone formation compared with wild-type MSCs. SHP1 was found to bind to GSK3 beta and suppress its kinase activity by dephosphorylating pY216, thus resulting in beta-catenin stabilization. Mice, in which SHP1 was deleted in MSCs using SHP1(fl/fl) Dermo1-cre, displayed significantly decreased bone mass and increased adipose tissue. Taken together, these results suggest a possible role for SHP1 in controlling tissue homeostasis through modulation of MSC differentiation via Wnt signaling regulation.

关 键 词：细胞分化 骨质疏松 酪氨酸 磷酸 蛋白 脂肪细胞 成骨细胞 酶 

分 类 号：Q813[生物学—生物工程]