Up-regulation of PTEN (Phosphatase and Tensin Homolog Deleted on Chromosome Ten) Mediates p38 MAPK Stress Signal-induced Inhibition of Insulin Signaling

• DOI: 10.1074/jbc.m511105200
• Publication Date: 2006-01-18T03:02:30Z
• Authors: Ying H. Shen; Lin Zhang; Yehua Gan; Xinwen Wang; Jian Wang; Scott A. LeMaire; Joseph S. Coselli; Xing Li Wang
• Keywords: Tensin; Resistin

The key feature of metabolic syndrome, a cluster and cardiovascular disorders, is systemic insulin resistance, which associated with dysregulated endothelial nitric-oxide synthase (eNOS). Stress signaling induced by inflammation can inhibit signaling. However, molecular mechanisms for the cross-talk between stress resistance are only partially understood. Resistin, an adipokine/cytokine, involved in inflammatory processes that could lead to status vascular diseases. In current study, we observed resistin inhibited eNOS activation cells. Up-regulation PTEN (phosphatase tensin homolog deleted on chromosome ten) expression may mediate inhibitory effects. Activated p38 MAPK, but not JNK, up-regulation. We further found target transcriptional factor activating transcription factor-2 (ATF-2) bound ATF sites promoter. phosphorylation/activation ATF-2 its binding promoter were increased treatment. summary, up-regulation effects Resistin induces pathway, activate ATF-2, turn expression. Our findings suggest resistin-mediated inhibition contribute