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Text
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URL Address
<a href="http://doi.org/10.1152/ajpheart.00421.2002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00421.2002</a>
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Pages
H176-H184
Issue
1
Volume
284
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Title
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Aldosterone stimulates proliferation of cardiac fibroblasts by activating Ki-RasA and MAPK1/2 signaling
Publisher
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American Journal of Physiology-Heart and Circulatory Physiology
Date
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2003
2003-01
Subject
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angiotensin-ii; Cardiovascular System & Cardiology; differentiation; fibrosis; gene-expression; Heart failure; identification; induction; Kirsten Ras; mineralocorticoid; mitogen-activated protein kinase; myofibroblast; na+ reabsorption; Physiology; receptor; spironolactone; transcription
Creator
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Stockand J D; Meszaros J G
Description
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Aldosterone plays a pathological role in cardiac fibrosis by directly affecting cardiac fibroblasts. Understanding of the cellular mechanisms of aldosterone action in cardiac fibroblasts, however, is rudimentary. One possibility is that aldosterone promotes proliferation of cardiac fibroblasts by activating specific cellular signaling cascades. The current study tests whether aldosterone stimulates proliferation of isolated adult rat cardiac myofibroblasts (RCF) by activating Kirsten Ras (Ki-RasA) and its effector, the MAPK1/2 cascade. Aldosterone (10 nM) significantly increased RCF proliferation. This action was sensitive to the mineralocorticoid receptor (MR) antagonist spironolactone. Expression of MR in RCF and the whole rat heart was confirmed by immunoblotting. Aldosterone significantly increased absolute and active (GTP bound) Ki-RasA levels in RCF. Aldosterone, in addition, significantly increased phospho-c-Raf and phospho-MAPK1/2. The effects of aldosterone on Ki-RasA and phospho-c-Raf proteins were inhibited by spironolactone but not RU-486, suggesting that aldosterone acts via MR. Inhibitors of MEK1/2 and c-Raf prevented aldosterone-induced activation of MAPK1/2 and proliferation. These results show that aldosterone directly increases RCF proliferation through MR-dependent activation of Ki-RasA and its effector, the MAPK1/2 cascade. Activation of cardiac fibroblasts through such a cascade may play a role in the pathological actions exerted by aldosterone on the heart.
Identifier
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<a href="http://doi.org/10.1152/ajpheart.00421.2002" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00421.2002</a>
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Journal Article
2003
American Journal of Physiology-Heart and Circulatory Physiology
angiotensin-ii
Cardiovascular System & Cardiology
differentiation
Fibrosis
gene-expression
Heart failure
identification
induction
Journal Article
Kirsten Ras
Meszaros J G
mineralocorticoid
mitogen-activated protein kinase
myofibroblast
na+ reabsorption
Physiology
Receptor
spironolactone
Stockand J D
Transcription