SHP1 Regulates Bone Mass by Directing Mesenchymal Stem Cell Differentiation | Zendy

Menghui Jiang | Zendy; Chunxing Zheng | Zendy; Peishun Shou | Zendy; Na Li | Zendy; Gang Cao | Zendy; Qing Chen | Zendy; Chunliang Xu | Zendy; Liming Du | Zendy; Qian Yang | Zendy; Jianchang Cao | Zendy; Yanyan Han | Zendy; Fengying Li | Zendy; Wei Cao | Zendy; Feng Liu | Zendy; Arnold B. Rabson | Zendy; Arthur I. Roberts | Zendy; WeiFen Xie | Zendy; Ying Wang | Zendy; Yufang Shi | Zendy

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SHP1 Regulates Bone Mass by Directing Mesenchymal Stem Cell Differentiation

Author(s) -

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,

Ying Wang,

Yufang Shi

Publication year - 2016

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2016.06.035

Subject(s) - mesenchymal stem cell , adipogenesis , wnt signaling pathway , adipose tissue , microbiology and biotechnology , chemistry , stem cell , alkaline phosphatase , endocrinology , biology , medicine , cancer research , signal transduction , biochemistry , enzyme

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 GSK3β and suppress its kinase activity by dephosphorylating pY216, thus resulting in β-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.

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