Abstract:
AIMS:In response to vascular injury, vascular smooth muscle cells (VSMC) may change from a contractile phenotype to a proliferative phenotype and consequently become conducive to neointima formation. Apoptosis repressor with caspase recruitment domain (ARC) was initially discovered as an endogenous apoptosis inhibitor, but whether ARC plays a role in VSMCs and whether it can participate in the regulation of atherosclerosis are unknown. METHODS AND RESULTS:Protein and mRNA levels of ARC in tissues and cells were detected by western blot and quantitative real-time PCR. Immunofluorescence staining was used to detect the protein location, and immunohistochemistry was used to detect protein expression in tissues. VSMC proliferation was analysed using Cell Counting Kit-8 (CCK-8) and EdU assays, while migration was assessed by Transwell assay. Mechanistically, the direct binding between two proteins was verified by immunoprecipitation. We found that ARC expression was stimulated in VSMCs during cell proliferation. Our results also showed that ARC promoted cell proliferation and induced phenotypic modulation of VSMCs in vitro and vivo. Mechanistic studies demonstrated that ARC increased the nuclear localization of Yes associated protein (YAP) by binding to 14-3-3ε and that ARC played a role in promoting cell proliferation and phenotypic modulation. Additionally, the transcription factor p53 negatively regulated ARC expression at the transcriptional level during cell proliferation and phenotypic modulation. CONCLUSIONS:Our findings define a novel role for ARC in the phenotypic transition of proliferating VSMCs, which may provide a new strategy for regulating neointimal formation.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Liu M,Yu T,Li M,Fang X,Hou B,Liu G,Wang Jdoi
10.1016/j.yjmcc.2020.08.003subject
Has Abstractpub_date
2020-10-01 00:00:00pages
35-48eissn
0022-2828issn
1095-8584pii
S0022-2828(20)30241-8journal_volume
147pub_type
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journal_title:Journal of molecular and cellular cardiology
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journal_title:Journal of molecular and cellular cardiology
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journal_title:Journal of molecular and cellular cardiology
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journal_title:Journal of molecular and cellular cardiology
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doi:10.1016/j.yjmcc.2016.05.013
更新日期:2016-08-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2008.06.010
更新日期:2008-09-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/0022-2828(89)90795-5
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2010.05.013
更新日期:2010-11-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1006/jmcc.1999.1087
更新日期:2000-03-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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更新日期:1986-12-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/0022-2828(90)90981-7
更新日期:1990-12-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2018.10.022
更新日期:2018-12-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章,评审
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更新日期:2001-04-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1006/jmcc.1994.1084
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章,评审
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2011.12.007
更新日期:2012-03-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章,评审
doi:10.1016/j.yjmcc.2009.09.001
更新日期:2010-03-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/s0022-2828(84)80040-1
更新日期:1984-12-01 00:00:00
abstract::The aim of this study was to investigate the effects of aging on the profile of myocardial substrate utilization and cardiac function using a physiological profile of substrates. Hearts from 6-, 15- and 24-month male Wistar rats were perfused in the isovolumic Langendorff mode, with physiological concentrations of 13C...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2005.09.018
更新日期:2006-01-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2020.03.013
更新日期:2020-06-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1006/jmcc.1999.1043
更新日期:1999-12-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/0022-2828(92)91159-3
更新日期:1992-01-01 00:00:00
abstract::Activation of both mTOR and its downstream target, S6K1 (p70 S6 kinase) have been implicated to affect cardiac hypertrophy. Our earlier work, in a feline model of 1-48 h pressure overload, demonstrated that mTOR/S6K1 activation occurred primarily through a PKC/c-Raf pathway. To further delineate the role of specific P...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2007.09.015
更新日期:2007-12-01 00:00:00