Abnormal proliferation of vascular smooth muscle cells (VSMCs) contributes significantly to the pathogenesis
of atherosclerosis. MiR-10b has recently emerged as a critical mediator in regulating cell proliferation in many diseases.
In our study, miR-10b expression was up-regulated in VSMCs isolated from atherosclerotic plaques, as well as in PDGFstimulated
VSMCs.Overexpression of miR-10b promoted cell proliferation of VSMCs. Furthermore, we identified the
Tat-interacting protein 30 (TIP30) as a direct target gene of miR-10b. TIP30 was down-regulated in VSMCs isolated from
atherosclerosis plaques, as well as in proliferative VSMCs. Knockdown of TIP30 promoted VSMCs proliferation. In addition,
miR-10b induced TIP30 down-regulation was accompanied by increased Akt phosphorylation. Akt was critical for
miR-10b-mediated VSMCs proliferation. Our results demonstrated that miR-10b contributed to abnormal VSMCs proliferation
through inhibiting the Akt pathway by targeting TIP30 in atherosclerosis. The modulation of miR-10b in VSMCs
provides a potential target for the therapy of atherosclerosis.
Keywords: Atherosclerosis, vascular smooth muscle cells, mirna, mir-10b, proliferation, ip30.
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