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Prostaglandin E2 Inhibits TNFα-induced Apoptosis in Mouse Osteoblasts
Zhou-Qi Yang, Rui Meng, Zhe Wang, Wei Zhang, Peng Shang*
Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environmental Biophysics, Faculty of Life Sciences,Northwestern Polytechnical University, Xi’an 710072, China
Abstract: Previous studies have revealed that prostaglandin E2(PGE2) regulated the proliferation and differentiation of osteoblasts in the manner of autocrine or paracrine. In this study， the regulatory role of PGE2 on TNFα-induced apoptosis in primary mouse osteoblasts or osteoblast-like MC3T3-E1 cells was investigated. The results demonstrated that oscillatory fluid shear stress (OFSS) promoted the expression of cyclooxygenase-2 (COX- 2)， stimulated PGE2 secretion in culture media， and inhibited TNFα-induced apoptosis in primary osteoblasts and MC3T3-E1 cells. Application of COX-2 selective inhibitor NS-398 significanly enhanced TNFα-induced activation of caspase-3 in osteoblasts in a time-dependent manner. Hoechst 33258/PI staining experiment showed that NS-398 distinctly increased the membrane permeability and the chromatin condensation in osteoblasts， however， application of PGE2 suppressed this effect. Further investigation indicated that NS-398 increased the activity of caspase-3 induced by TNF-α in osteoblasts， and the addition of exogenous PGE2 in culture media restrained this effect. In conclusion， endogenous and exogenous PGE2 inbihits TNFα-induced apoptosis in mouse osteoblasts.
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