| First Author | Jiang M | Year | 2016 |
| Journal | Cell Rep | Volume | 16 |
| Issue | 3 | Pages | 769-80 |
| PubMed ID | 27396328 | Mgi Jnum | J:238679 |
| Mgi Id | MGI:5823344 | Doi | 10.1016/j.celrep.2016.06.035 |
| Citation | Jiang M, et al. (2016) SHP1 Regulates Bone Mass by Directing Mesenchymal Stem Cell Differentiation. Cell Rep 16(3):769-80 |
| abstractText | 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 GSK3beta 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. |
