| First Author | Cao J | Year | 2015 |
| Journal | Mol Cell Endocrinol | Volume | 410 |
| Pages | 27-34 | PubMed ID | 25666993 |
| Mgi Jnum | J:224184 | Mgi Id | MGI:5661644 |
| Doi | 10.1016/j.mce.2015.01.045 | Citation | Cao J, et al. (2015) Impact of targeted PPARgamma disruption on bone remodeling. Mol Cell Endocrinol 410:27-34 |
| abstractText | Peroxisome proliferator-activated receptor gamma (PPARgamma), known as the master regulator of adipogenesis, has been regarded as a promising target for new anti-osteoporosis therapy due to its role in regulating bone marrow mesenchymal stem/progenitor cell (BMSC) lineage commitment. However, the precise mechanism underlying PPARgamma regulation of bone is not clear as a bone-specific PPARgamma conditional knockout (cKO) study has not been conducted and evidence showed that deletion of PPARgamma in other tissues also have profound effect on bone. In this study, we show that mice deficiency of PPARgamma in cells expressing a 3.6 kb type I collagen promoter fragment (PPAR(fl/fl):Col3.6-Cre) exhibits a moderate, site-dependent bone mass phenotype. In vitro studies showed that adipogenesis is abolished completely and osteoblastogenesis increased significantly in both primary bone marrow culture and the BMSCs isolated from PPARgamma cKO mice. Histology and histomorphometry studies revealed significant increases in the numbers of osteoblasts and surface in the PPARgamma cKO mice. Finally, we found that neither the differentiation nor the function of osteoclasts was affected in the PPARgamma cKO mice. Together, our studies indicate that PPARgamma plays an important role in bone remodeling by increasing the abundance of osteoblasts for repair, but not during skeletal development. |
