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Nishimura, K. et al.

Nishimura, Setoyama, Tsumagari, Miyata, Hatano, Xu, Jisaka, Nagaya, Yokota,

Endogenous Prostaglandins E(2) and F(2(alpha)) Serve as an Anti-Apoptotic Factor against Apoptosis Induced by Tumor Necrosis Factor-alpha in Mouse 3T3-L1 Preadipocytes.

Adipocytes can function as endocrine cells secreting a variety of adipocytokines including tumor necrosis factor (TNF)-alpha. Treatment of cultured mouse 3T3-L1 preadipocytes with TNF-alpha induced apoptosis, as was evident from increases in nuclear condensation and caspase-3 activity, but differentiated adipocytes during the maturation phase showed resistance to apoptosis by TNF-alpha. Antioxidants effectively reduced TNF-alpha-induced apoptosis in preadipocytes, indicating the involvement of reactive oxygen species. Exposure of preadipocytes to calcium ionophore A23187 reduced TNF-alpha-induced apoptosis, which was accompanied by increased production of prostaglandins (PGs) E(2) and PGF(2(alpha)). TNF-alpha preferentially promoted gene expression of cyclooxygenase (COX)-2 without affecting that of COX-1. Consistently, NS-398, a COX-2 inhibitor, stimulated TNF-alpha-induced apoptosis, which was reversed by exogenous PGE(2) and PGF(2(alpha)). These results indicate that endogenous PGE(2) and PGF(2(alpha)) synthesized by preadipocytes through the induction of COX-2 can serve as anti-apoptotic factors against apoptosis by TNF-alpha.[1]

References

Endogenous Prostaglandins E(2) and F(2(alpha)) Serve as an Anti-Apoptotic Factor against Apoptosis Induced by Tumor Necrosis Factor-alpha in Mouse 3T3-L1 Preadipocytes. Nishimura, K., Setoyama, T., Tsumagari, H., Miyata, N., Hatano, Y., Xu, L., Jisaka, M., Nagaya, T., Yokota, K. Biosci. Biotechnol. Biochem. (2006) [Pubmed]

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