title: Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation.
abstract: 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.
authors.affiliation: Department of Cardiology, Zhongda Hospital of Southeast University Medical School, Nanjing, Jiangsu, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Qiao
authors.affiliation: Department of Cardiology, Zhongda Hospital of Southeast University Medical School, Nanjing, Jiangsu, China. Electronic address: tangchengchun@medmail.com.cn.
authors.forename: Chengchun
authors.initials: C
authors.lastname: Tang
authors.affiliation: Department of Cardiology, Zhongda Hospital of Southeast University Medical School, Nanjing, Jiangsu, China.
authors.forename: Qingjie
authors.initials: Q
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Zhongda Hospital of Southeast University Medical School, Nanjing, Jiangsu, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Zhongda Hospital of Southeast University Medical School, Nanjing, Jiangsu, China.
authors.forename: Gaoliang
authors.initials: G
authors.lastname: Yan
authors.affiliation: Department of Cardiology, Zhongda Hospital of Southeast University Medical School, Nanjing, Jiangsu, China.
authors.forename: Boqian
authors.initials: B
authors.lastname: Zhu
mesh_terms: D000818:Animals; D020212:Carotid Artery Injuries / Q000378:metabolism / Q000473:pathology*; D002465:Cell Movement / Q000502:physiology*; D049109:Cell Proliferation / Q000502:physiology*; D002478:Cells, Cultured; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000473:pathology / Q000502:physiology*; D058426:Neointima / Q000473:pathology / Q000503:physiopathology*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration / Q000502:physiology
chemical_list: C575188:KCNJ2 protein, rat; D024661:Potassium Channels, Inwardly Rectifying
keywords: Migration; Neointimal formation; Proliferation; Rectifier K(+) currents; Vascular smooth muscle cell