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FEBS Lett. 2012 Sep 21;586(19):3341-8. doi: 10.1016/j.febslet.2012.07.015. Epub 2012 Jul 20.

PC-PLC is involved in osteoclastogenesis induced by TNF-α through upregulating IP3R1 expression.

Author information

1
Institution of Dental Medicine, Shandong University, Jinan 250012, PR China.

Abstract

The precise mechanism of how TNF-α promotes osteoclast formation is not clear. Previous reports show TNF-α 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-α 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-α, 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-α promotes RANKL-induced osteoclastogenesis, at least partially, through PC-PLC/IP3R1/NFATc1 pathway.

PMID:
22819818
DOI:
10.1016/j.febslet.2012.07.015
[Indexed for MEDLINE]
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