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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{sup +} 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:
; ; ; ; ;
Publication Date:
OSTI Identifier:
22606187
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 477; Journal Issue: 4; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ACTIN; ARTERIOSCLEROSIS; CELL PROLIFERATION; CORONARIES; GROWTH FACTORS; INJURIES; KAONS PLUS; MUSCLES; PHENOTYPE; POTASSIUM IONS; RATS; RECTIFIERS

Citation Formats

Qiao, Yong, Tang, Chengchun, E-mail: tangchengchun@medmail.com.cn, Wang, Qingjie, Wang, Dong, Yan, Gaoliang, and Zhu, Boqian. Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation. United States: N. p., 2016. Web. doi:10.1016/J.BBRC.2016.06.134.
Qiao, Yong, Tang, Chengchun, E-mail: tangchengchun@medmail.com.cn, Wang, Qingjie, Wang, Dong, Yan, Gaoliang, & Zhu, Boqian. Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation. United States. doi:10.1016/J.BBRC.2016.06.134.
Qiao, Yong, Tang, Chengchun, E-mail: tangchengchun@medmail.com.cn, Wang, Qingjie, Wang, Dong, Yan, Gaoliang, and Zhu, Boqian. Fri . "Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation". United States. doi:10.1016/J.BBRC.2016.06.134.
@article{osti_22606187,
title = {Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation},
author = {Qiao, Yong and Tang, Chengchun, E-mail: tangchengchun@medmail.com.cn and Wang, Qingjie and Wang, Dong and Yan, Gaoliang and Zhu, Boqian},
abstractNote = {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{sup +} 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.},
doi = {10.1016/J.BBRC.2016.06.134},
journal = {Biochemical and Biophysical Research Communications},
number = 4,
volume = 477,
place = {United States},
year = {Fri Sep 02 00:00:00 EDT 2016},
month = {Fri Sep 02 00:00:00 EDT 2016}
}