Abstract
Restenosis formation is initiated from intimal hyperplasia when arterial stretch and injury exist. In this study, we examined the role of CDKN1A-interacting zinc finger protein 1 (CIZ1) in neointimal hyperplasia in injured arteries. CIZ1 protein was up-regulated, and p21Cip1/Waf1 (p21) was down-regulated in the neointimal hyperplasia from a mouse femoral artery wire-injury model. In vitro, proliferation and migration were reduced in vascular smooth muscle cells transformed with Ciz1-shRNA lentiviral particles. In addition, p21 expression is increased, and MMP9 expression is decreased in vascular smooth muscle cells with CIZ1 knockdown. These data imply that CIZ1 might be a novel repressor of neointimal lesion formation caused by interventional therapy.
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