| First Author | Sang C | Year | 2016 |
| Journal | Bone | Volume | 84 |
| Pages | 78-87 | PubMed ID | 26723579 |
| Mgi Jnum | J:230879 | Mgi Id | MGI:5766410 |
| Doi | 10.1016/j.bone.2015.12.012 | Citation | Sang C, et al. (2016) Tumor necrosis factor alpha suppresses osteogenic differentiation of MSCs by inhibiting semaphorin 3B via Wnt/beta-catenin signaling in estrogen-deficiency induced osteoporosis. Bone 84:78-87 |
| abstractText | The proinflammatory cytokines, especially tumor necrosis factor alpha (TNF-alpha), have been shown to inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and bone formation in estrogen-deficiency-induced osteoporosis, but the mechanisms of TNF-alpha impaired bone formation remain poorly understood. Semaphorins have been shown to regulate cell growth, cell migration, and cell differentiation in a variety of tissues, including bone tissue. Here, we identified a novel mechanism whereby TNF-alpha, suppressing Semaphorin3B expression contributes to estrogen-deficiency-induced osteoporosis. In this study, we found that TNF-alpha could decrease Semaphorin3B expression in osteogenic differentiation of MSCs. Overexpression of Semaphorin3B in MSCs attenuated the inhibitory effects of TNF-alpha on MSCs proliferation and osteoblastic differentiation. Mechanistically, activation of the Wnt/beta-catenin signaling markedly rescued TNF-alpha-inhibited Semaphorin3B expression, suggesting that Wnt/beta-catenin signaling was involved in the regulation of Semaphorin3B expression by TNF-alpha. Taken together, our results revealed a novel function for Semaphorin3B and suggested that suppressed Semaphorin3B may contribute to impaired bone formation by elevated TNF-alpha in estrogen-deficiency-induced osteoporosis. This study may indicate a therapeutic target gene of Semaphorin3B for osteoporosis. |
