| First Author | Xia L | Year | 2012 |
| Journal | FEBS Lett | Volume | 586 |
| Issue | 19 | Pages | 3341-8 |
| PubMed ID | 22819818 | Mgi Jnum | J:188494 |
| Mgi Id | MGI:5440777 | Doi | 10.1016/j.febslet.2012.07.015 |
| Citation | Xia L, et al. (2012) PC-PLC is involved in osteoclastogenesis induced by TNF-alpha through upregulating IP3R1 expression. FEBS Lett 586(19):3341-8 |
| abstractText | The precise mechanism of how TNF-alpha promotes osteoclast formation is not clear. Previous reports show TNF-alpha targets molecules that regulate calcium signaling. Inositol-1,4,5-trisphosphate receptors (IP3Rs) are important calcium channel responsible for evoking intracellular calcium oscillation. We found that TNF-alpha increased the expression of IP3R1 and promoted osteoclastogenesis in RANKL-induced mouse BMMs. Phosphatidylcholine-specific phospholipase C (PC-PLC) specific inhibitor D609 eliminated the upregulation of IP3R1 by TNF-alpha, and decreased the autoamplification of nuclear factor of activated T-cells 1 (NFATc1), thus resulted in less osteoclasts formation. However, D609 did not inhibit RANKL-induced osteoclastogenesis. Our data suggest TNF-alpha promotes RANKL-induced osteoclastogenesis, at least partially, through PC-PLC/IP3R1/NFATc1 pathway. |
