Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation

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• 作者：Yong Qiao ; Chengchun Tang ; ^{tangchengchun@medmail.com.cn" class="auth_mail" title="E-mail the corresponding author} ; Qingjie Wang ; Dong Wang ; Gaoliang Yan ; Boqian Zhu
• 关键词：Rectifier K+ currents ; Vascular smooth muscle cell ; Proliferation ; Migration ; Neointimal formation
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2016
• 出版时间：2 September 2016
• 年：2016
• 卷：477
• 期：4
• 页码：774-780
• 全文大小：1380 K

文摘

Phenotype switching of vascular smooth muscle cells (VSMC) from the contractile type to the synthetic type is a hallmark of vascular disorders such as atherosclerosis and restenosis after angioplasty. Inward rectifier K⁺ channel 2.1 (Kir2.1) has been identified in VSMC. However, whether it plays a functional role in regulating cellular transformation remains obscure. In this study, we evaluated the role of Kir2.1 on VSMC proliferation, migration, phenotype switching, and post-injury carotid neointimal formation. Kir2.1 knockdown significantly suppressed platelet-derived growth factor BB-stimulated rat vascular smooth muscle cells (rat-VSMC) proliferation and migration. Deficiency in Kir2.1 contributed to the restoration of smooth muscle α-actin, smooth muscle 22α, and calponin and to a reduction in osteopontin expression in rat-VSMC. Moreover, the in vivo study showed that rat-VSMC switched to proliferative phenotypes and that knockdown of Kir2.1 significantly inhibited neointimal formation after rat carotid injury. Kir2.1 may be a potential therapeutic target in the treatment of cardiovascular diseases, such as atherosclerosis and restenosis following percutaneous coronary intervention.