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Epicardial adipose tissue is able to synthesize and secrete adipokines which play important roles in atherosclerosis. WISP1 (Wnt1 inducible signaling pathway protein 1, CCN4) is a novel adipokine which act on artery wall layers through vasocrine and/or paracrine functions. The role of WISP1 in atherosclerosis is not clear. Since increased vascular smooth muscle cells (VSMCs) apoptosis within the plaque is associated with plaque instability, we focused on whether WISP1 can protect vascular smooth muscle cells from H2O2-induced apoptosis and the possible mechanism of it.
First, we treated VSMCs with/or without WISP1, then we detected the expression of MEK/ERK pathway related proteins in each group of VSMCs. Next we examined the effects of H2O2 on each group of VSMCs using TUNEL staining and caspase3. Moreover we treated VSMCs with both MEK inhibitor and WISP1, then tested the expression of MEK/ERK pathway related proteins and the effect of H2O2 on VSMCs again.
WISP1 upregulated the MEK/ERK pathway by increasing the phosphorylation of MEK and ERK. Pre-treatment of WISP1 inhibited H2O2 induced VSMCs apoptosis. Additionally, blockade of MEK/ERK pathway dampened the anti-apoptotic effect of WISP1.
In this study, we elucidates that WISP1 protects VSMCs from H2O2-induced apoptosis through the MEK/ERK pathway, which means that enhanced WISP1 expression and secretion may provide protective effects on plaque by inhibiting VSMCs apoptosis.