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Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity

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Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity. / Chen, Lihua; DeWispelaere, Allison; Dastvan, Frank; Osborne, William R A; Blechner, Christine; Windhorst, Sabine; Daum, Guenter.

In: PLOS ONE, Vol. 11, No. 5, 2016, p. e0155726.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Chen, L, DeWispelaere, A, Dastvan, F, Osborne, WRA, Blechner, C, Windhorst, S & Daum, G 2016, 'Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity', PLOS ONE, vol. 11, no. 5, pp. e0155726. https://doi.org/10.1371/journal.pone.0155726

APA

Chen, L., DeWispelaere, A., Dastvan, F., Osborne, W. R. A., Blechner, C., Windhorst, S., & Daum, G. (2016). Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity. PLOS ONE, 11(5), e0155726. https://doi.org/10.1371/journal.pone.0155726

Vancouver

Chen L, DeWispelaere A, Dastvan F, Osborne WRA, Blechner C, Windhorst S et al. Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity. PLOS ONE. 2016;11(5):e0155726. https://doi.org/10.1371/journal.pone.0155726

Bibtex

@article{6f16eaab0ce04eeca1d5cd06b902e11e,
title = "Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity",
abstract = "Smooth muscle alpha-actin (SMA) is a marker for the contractile, non-proliferative phenotype of adult smooth muscle cells (SMCs). Upon arterial injury, expression of SMA and other structural proteins decreases and SMCs acquire a pro-migratory and proliferative phenotype. To what extent SMA regulates migration and proliferation of SMCs is unclear and putative signaling pathways involved remain to be elucidated. Here, we used lentiviral-mediated gene transfer and siRNA technology to manipulate expression of SMA in carotid mouse SMCs and studied effects of SMA. Overexpression of SMA results in decreased proliferation and migration and blunts serum-induced activation of the small GTPase Rac, but not RhoA. All inhibitory effects of SMA are rescued by expression of a constitutively active Rac1 mutant (V12rac1). Moreover, reduction of SMA expression by siRNA technology results in an increased activation of Rac. Taken together, this study identifies Rac1 as a downstream target for SMA to inhibit SMC proliferation and migration.",
keywords = "Journal Article",
author = "Lihua Chen and Allison DeWispelaere and Frank Dastvan and Osborne, {William R A} and Christine Blechner and Sabine Windhorst and Guenter Daum",
year = "2016",
doi = "10.1371/journal.pone.0155726",
language = "English",
volume = "11",
pages = "e0155726",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "5",

}

RIS

TY - JOUR

T1 - Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity

AU - Chen, Lihua

AU - DeWispelaere, Allison

AU - Dastvan, Frank

AU - Osborne, William R A

AU - Blechner, Christine

AU - Windhorst, Sabine

AU - Daum, Guenter

PY - 2016

Y1 - 2016

N2 - Smooth muscle alpha-actin (SMA) is a marker for the contractile, non-proliferative phenotype of adult smooth muscle cells (SMCs). Upon arterial injury, expression of SMA and other structural proteins decreases and SMCs acquire a pro-migratory and proliferative phenotype. To what extent SMA regulates migration and proliferation of SMCs is unclear and putative signaling pathways involved remain to be elucidated. Here, we used lentiviral-mediated gene transfer and siRNA technology to manipulate expression of SMA in carotid mouse SMCs and studied effects of SMA. Overexpression of SMA results in decreased proliferation and migration and blunts serum-induced activation of the small GTPase Rac, but not RhoA. All inhibitory effects of SMA are rescued by expression of a constitutively active Rac1 mutant (V12rac1). Moreover, reduction of SMA expression by siRNA technology results in an increased activation of Rac. Taken together, this study identifies Rac1 as a downstream target for SMA to inhibit SMC proliferation and migration.

AB - Smooth muscle alpha-actin (SMA) is a marker for the contractile, non-proliferative phenotype of adult smooth muscle cells (SMCs). Upon arterial injury, expression of SMA and other structural proteins decreases and SMCs acquire a pro-migratory and proliferative phenotype. To what extent SMA regulates migration and proliferation of SMCs is unclear and putative signaling pathways involved remain to be elucidated. Here, we used lentiviral-mediated gene transfer and siRNA technology to manipulate expression of SMA in carotid mouse SMCs and studied effects of SMA. Overexpression of SMA results in decreased proliferation and migration and blunts serum-induced activation of the small GTPase Rac, but not RhoA. All inhibitory effects of SMA are rescued by expression of a constitutively active Rac1 mutant (V12rac1). Moreover, reduction of SMA expression by siRNA technology results in an increased activation of Rac. Taken together, this study identifies Rac1 as a downstream target for SMA to inhibit SMC proliferation and migration.

KW - Journal Article

U2 - 10.1371/journal.pone.0155726

DO - 10.1371/journal.pone.0155726

M3 - SCORING: Journal article

C2 - 27176050

VL - 11

SP - e0155726

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 5

ER -