Downregulation of miR‐21 is Involved in Direct Actions of Ursolic Acid on the Heart: Implications for Cardiac Fibrosis and Hypertrophy. Issue 4 (7th July 2015)
- Record Type:
- Journal Article
- Title:
- Downregulation of miR‐21 is Involved in Direct Actions of Ursolic Acid on the Heart: Implications for Cardiac Fibrosis and Hypertrophy. Issue 4 (7th July 2015)
- Main Title:
- Downregulation of miR‐21 is Involved in Direct Actions of Ursolic Acid on the Heart: Implications for Cardiac Fibrosis and Hypertrophy
- Authors:
- Dong, Xingli
Liu, Shangkun
Zhang, Lingling
Yu, Siming
Huo, Linman
Qile, Muge
Liu, Lu
Yang, Baofeng
Yu, Jinling - Abstract:
- <abstract abstract-type="main" id="cdr12125-abs-0001"> <title>Summary</title> <sec id="cdr12125-sec-0001" sec-type="section"> <title>Purpose</title> <p>Myocardial fibrosis contributes to cardiac remodeling and loss of cardiac function in myocardial infarction and heart failure. This study used <italic>in vitro</italic> and <italic>in vivo</italic> models to examine the effects of ursolic acid (UA) on myocardial fibrosis and to explore its potential mechanism.</p> </sec> <sec id="cdr12125-sec-0002" sec-type="section"> <title>Methods</title> <p>Transverse aortic constriction (TAC) surgery was performed in mice to induce cardiac hypertrophy and fibrosis. UA was orally administered 1 week prior to TAC. Two weeks after TAC, myocardial pathology was detected using Masson's trichrome staining and transmission electron microscopy, and heart‐to‐body weight ratio was measured. For <italic>in vitro</italic> studies, cultured cardiac fibroblasts were treated with serum in the presence or absence of UA. The relative levels of miR‐21 and p‐ERK/ERK, collagen content and cell viability were measured.</p> </sec> <sec id="cdr12125-sec-0003" sec-type="section"> <title>Results</title> <p>Ursolic acid attenuated pathological cardiac hypertrophy and myocardial fibrosis <italic>in vivo</italic> induced by TAC. Downregulation of miR‐21 and p‐ERK/ERK were observed in myocardial fibroblasts treated with UA in a dose‐dependent manner compared with the control group both <italic>in vitro</italic> and<abstract abstract-type="main" id="cdr12125-abs-0001"> <title>Summary</title> <sec id="cdr12125-sec-0001" sec-type="section"> <title>Purpose</title> <p>Myocardial fibrosis contributes to cardiac remodeling and loss of cardiac function in myocardial infarction and heart failure. This study used <italic>in vitro</italic> and <italic>in vivo</italic> models to examine the effects of ursolic acid (UA) on myocardial fibrosis and to explore its potential mechanism.</p> </sec> <sec id="cdr12125-sec-0002" sec-type="section"> <title>Methods</title> <p>Transverse aortic constriction (TAC) surgery was performed in mice to induce cardiac hypertrophy and fibrosis. UA was orally administered 1 week prior to TAC. Two weeks after TAC, myocardial pathology was detected using Masson's trichrome staining and transmission electron microscopy, and heart‐to‐body weight ratio was measured. For <italic>in vitro</italic> studies, cultured cardiac fibroblasts were treated with serum in the presence or absence of UA. The relative levels of miR‐21 and p‐ERK/ERK, collagen content and cell viability were measured.</p> </sec> <sec id="cdr12125-sec-0003" sec-type="section"> <title>Results</title> <p>Ursolic acid attenuated pathological cardiac hypertrophy and myocardial fibrosis <italic>in vivo</italic> induced by TAC. Downregulation of miR‐21 and p‐ERK/ERK were observed in myocardial fibroblasts treated with UA in a dose‐dependent manner compared with the control group both <italic>in vitro</italic> and <italic>in vivo</italic>.</p> </sec> <sec id="cdr12125-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Our study demonstrates that UA can inhibit myocardial fibrosis both <italic>in vitro</italic> and <italic>in vivo</italic>, and the effects of UA on myocardial fibrosis may be due to the inhibition of miR‐21/ERK signaling pathways.</p> </sec> </abstract> … (more)
- Is Part Of:
- Cardiovascular therapeutics. Volume 33:Issue 4(2015:Aug.)
- Journal:
- Cardiovascular therapeutics
- Issue:
- Volume 33:Issue 4(2015:Aug.)
- Issue Display:
- Volume 33, Issue 4 (2015)
- Year:
- 2015
- Volume:
- 33
- Issue:
- 4
- Issue Sort Value:
- 2015-0033-0004-0000
- Page Start:
- 161
- Page End:
- 167
- Publication Date:
- 2015-07-07
- Subjects:
- Cardiovascular pharmacology -- Periodicals
Cardiovascular agents -- Periodicals
Cardiovascular system -- Diseases -- Chemotherapy -- Periodicals
Cardiovascular Agents -- Periodicals
Cardiovascular Diseases -- drug therapy -- Periodicals
Agents cardiovasculaires -- Périodiques
Appareil cardiovasculaire -- Maladies -- Chimiothérapie -- Périodiques
616.1005 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1755-5922 ↗
http://www.blackwell-synergy.com/loi/cath ↗
http://www.blackwellpublishing.com/journal.asp?ref=1755-5914&site=1 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/1755-5922.12125 ↗
- Languages:
- English
- ISSNs:
- 1755-5914
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3051.520500
British Library HMNTS - ELD Digital store - Ingest File:
- 4221.xml