PMID- 24392114
OWN - NLM
STAT- MEDLINE
DCOM- 20141118
LR  - 20220408
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 1
DP  - 2014
TI  - MicroRNA-208a increases myocardial fibrosis via endoglin in volume overloading 
      heart.
PG  - e84188
LID - 10.1371/journal.pone.0084188 [doi]
LID - e84188
AB  - MicroRNA-208a (mir-208a) is essential for cardiac hypertrophy and fibrosis. 
      Endoglin, a co-receptor of transforming growth factor-beta is also essential for 
      cardiac fibrosis. Endoglin has been shown to be a target of mir-208a in the in 
      vitro mechanical stress model. Volume overload can lead to heart failure and 
      cardiac fibrosis. The role of mir-208a and endoglin in volume overload heart 
      failure is well known. We sought to investigate the mechanism of regulation of 
      mir-208a and endoglin in volume overload-induced heart failure. Aorta-caval (AV) 
      shunt was performed in adult Sprague-Dawley rats to induce volume overload. Heart 
      weight and heart weight/body weight ratio significantly increased in AV shunt 
      animals. AV shunt significantly increased left ventricular end-diastolic 
      dimension as compared to sham group. Mir-208a was significantly induced by AV 
      shunt from 3 to 14 days. Endoglin, myosin heavy chain-beta and brain natriuretic 
      peptide were significantly induced by AV shunt from 3 to 14 days. Overexpression 
      of mir-208a in the sham group without AV shunt significantly increased endoglin 
      expression similar to the AV shunt group. Antagomir-208a attenuated the endoglin 
      expression induced by AV shunt. Pretreatment with atorvastatin also attenuated 
      the endoglin expression induced by AV shunt. AV shunt significantly increased 
      myocardial fibrosis as compared to sham group. Overexpression of mir-208a in the 
      sham group significantly increased myocardial fibrosis. Antagomir-208a and 
      atorvastatin significantly attenuated the myocardial fibrosis induced by AV 
      shunt. In conclusion, mir-208a increased endoglin expression to induce myocardial 
      fibrosis in volume overloaded heart failure. Treatment with atorvastatin can 
      attenuate the myocardial fibrosis induced by volume overload through inhibition 
      of endoglin expression.
FAU - Wang, Bao-Wei
AU  - Wang BW
AD  - School of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan ; 
      Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwa.
FAU - Wu, Gong-Jhe
AU  - Wu GJ
AD  - School of Medicine, College of Medicine, Taipei Medical University, Taipei, 
      Taiwan ; Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, 
      Taipei, Taiwan.
FAU - Cheng, Wen-Ping
AU  - Cheng WP
AD  - Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwa.
FAU - Shyu, Kou-Gi
AU  - Shyu KG
AD  - Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwa ; 
      Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, 
      Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140102
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Endoglin)
RN  - 0 (Eng protein, rat)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (MIRN208 microRNA, rat)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Cardiomegaly/*genetics/*pathology/physiopathology
MH  - Disease Models, Animal
MH  - Echocardiography
MH  - Endoglin
MH  - Fibrosis
MH  - Gene Expression
MH  - Gene Expression Regulation
MH  - Hemodynamics
MH  - Intracellular Signaling Peptides and Proteins/*genetics
MH  - MicroRNAs/*genetics
MH  - Myocardium/*metabolism/*pathology
MH  - Organ Size
MH  - Rats
PMC - PMC3879305
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/01/07 06:00
MHDA- 2014/11/19 06:00
PMCR- 2014/01/02
CRDT- 2014/01/07 06:00
PHST- 2013/08/26 00:00 [received]
PHST- 2013/11/13 00:00 [accepted]
PHST- 2014/01/07 06:00 [entrez]
PHST- 2014/01/07 06:00 [pubmed]
PHST- 2014/11/19 06:00 [medline]
PHST- 2014/01/02 00:00 [pmc-release]
AID - PONE-D-13-35191 [pii]
AID - 10.1371/journal.pone.0084188 [doi]
PST - epublish
SO  - PLoS One. 2014 Jan 2;9(1):e84188. doi: 10.1371/journal.pone.0084188. eCollection 
      2014.