tailieunhanh - Báo cáo khoa học: 3T3-L1 adipocyte apoptosis induced by thiazolidinediones is peroxisome proliferator-activated receptor-c-dependent and mediated by the caspase-3-dependent apoptotic pathway

Although thiazolidinediones (TZDs) are potent promoters of adipogenesis in the preadipocyte, they induce apoptosis in several other cell types, such as cancer cells, endothelial cells and T-lymphocytes. In this study, we investigated the proapoptotic effect of TZDs in mature 3T3-L1 adipocytes, which express high levels of the peroxisome proliferator-acti-vated receptor-c (PPARc) protein. | 3T3-L1 adipocyte apoptosis induced by thiazolidinediones is peroxisome proliferator-activated receptor-y-dependent and mediated by the caspase-3-dependent apoptotic pathway Yuanyuan Xiao Taichang Yuan Wenqi Yao and Kan Liao State Key Laboratory of Molecular Biology Institute of Biochemistry and CellBiology Shanghai Institutes for BiologicalSciences Chinese Academy of Sciences Shanghai China Keywords 3T3-L1 adipocyte adipocyte apoptosis Akt-1 PPARc thiazolidinediones Correspondence K. Liao Institute of Biochemistry and Cell Biology 320 Yueyang Road Shanghai 200031 China Fax 86 21 54921011 Tel 86 21 54921113 E-mail kliao@ Received 11 March 2009 revised 16 November 2009 accepted 24 November 2009 doi Although thiazolidinediones TZDs are potent promoters of adipogenesis in the preadipocyte they induce apoptosis in several other cell types such as cancer cells endothelial cells and T-lymphocytes. In this study we investigated the proapoptotic effect of TZDs in mature 3T3-L1 adipocytes which express high levels of the peroxisome proliferator-acti-vated receptor-c PPARc protein. Apoptosis was induced in mature 3T3-L1 adipocytes by treatment with troglitazone pioglitazone or prostaglandin J2 and could be blocked by the PPARy antagonist GW9662. Treatment with PPARc agonists also decreased Akt-1 protein and phosphorylation levels without affecting phosphoinositide 3-kinase and PTEN. Further analysis indicated that in troglitazone-treated 3T3-L1 adipocytes Bad phosphorylation and Bcl-2 protein levels were reduced and Bax translocation to the mitochondria was increased. Subsequently cytochrome c release and caspase-3 cleavage were observed. TZD-induced adipocyte apoptosis could be blocked by the caspase-3 inhibitor Ac-DEVD-CHO or by overexpression of Bcl2. In cultured rat primary adipocytes similar apoptosis-inducing effects of troglitazone were also observed. Thus TZDs promote apoptosis in adipocytes through a PPARc-dependent pathway.

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