A novel reciprocal loop between microRNA-21 and TGFβRIII is involved in cardiac fibrosis

Liang, Haihai; Zhang, Chun; Ban, Takahiko; Liu, Yu; Liu, Mei; Piao, Xianmei; Zhao, Daqing; Lu, Yanjie; Chu, Wenfeng; Yang, Baofeng

doi:10.1016/j.biocel.2012.08.019

Cited by 148 publications

(120 citation statements)

References 37 publications

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“…Under H 2 O 2 conditions, an increase in TGFβR3 levels exerts a cumulative effect on the degree of apoptosis. Consistently, TGFβR3 is also known to enhance apoptosis in some tumor cells; however, TGFβR3 suppresses the apoptosis of cardiofibroblasts,7, 10 potentially by deactivating the TGFβR1/TGFβR2 complex to downregulate cell apoptosis 24. According to our data, TGFβR3 promotes cardiomyocyte apoptosis induced by myocardial infarction.…”

Section: Discussionsupporting

confidence: 84%

“…We demonstrated that overexpression of TGFβR3 during MI activates the p38 signaling pathway but does not alter the JNK1/2 or ERK1/2 pathway. Interestingly, TGFβR3‐induced activation of p38 signaling has also been detected in colon cancer cells, fibroblasts, and L6 myoblasts 24, 25. In the infarct heart, cytokines such as tumor necrosis factor and interleukin 6 and injury of ischemia‐reperfusion activate the p38 signaling pathway 26.…”

Section: Discussionmentioning

confidence: 99%

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Transforming Growth Factor‐β Receptor III is a Potential Regulator of Ischemia‐Induced Cardiomyocyte Apoptosis

Sun

Duan

et al. 2017

JAHA

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BackgroundMyocardial infarction (MI) is often accompanied by cardiomyocyte apoptosis, which decreases heart function and leads to an increased risk of heart failure. The aim of this study was to examine the effects of transforming growth factor‐β receptor III (TGFβR3) on cardiomyocyte apoptosis during MI.Methods and ResultsAn MI mouse model was established by left anterior descending coronary artery ligation. Cell viability, apoptosis, TGFβR3, and mitogen‐activated protein kinase signaling were assessed by methylthiazolyldiphenyl‐tetrazolium bromide assay, terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling assay, immunofluorescence, electron microscopy, and Western blotting. Our results demonstrated that TGFβR3 expression in the border region of the heart was dynamically changed during MI. After stimulation with H2O2, TGFβR3 overexpression in cardiomyocytes led to increased cell apoptosis and activation of p38 signaling, whereas TGFβR3 knockdown had the opposite effect. ERK1/2 and JNK1/2 signaling was not altered by TGFβR3 modulation, and p38 inhibitor (SB203580) reduced the effect of TGFβR3 on apoptosis, suggesting that p38 has a nonredundant function in activating apoptosis. Consistent with the in vitro observations, cardiac TGFβR3 transgenic mice showed augmented cardiomyocyte apoptosis, enlarged infarct size, increased injury, and enhanced p38 signaling upon MI. Conversely, cardiac loss of function of TGFβR3 by adeno‐associated viral vector serotype 9–TGFβR3 short hairpin RNA attenuated the effects of MI in mice.Conclusions TGFβR3 promotes apoptosis of cardiomyocytes via a p38 pathway–associated mechanism, and loss of TGFβR3 reduces MI injury, which suggests that TGFβR3 may serve as a novel therapeutic target for MI.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Transforming Growth Factor‐β Receptor III is a Potential Regulator of Ischemia‐Induced Cardiomyocyte Apoptosis

Sun

Duan

et al. 2017

JAHA

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“…while inducing the proliferation of fibroblasts, miR-21 simultaneously increases matrix deposition. Notably, miR-21 itself is upregulated by Tgf-β [91]. Also, miR-24 and miR-101 have been suggested to influence Tgf-β pathway.…”

Section: Fibroblast Proliferation and Activation: Fibrosismentioning

confidence: 99%

MicroRNAs in myocardial ischemia: identifying new targets and tools for treating heart disease. New frontiers for miR-medicine

Sala

Bergerone

Gatti

et al. 2013

Cell. Mol. Life Sci.

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“…Liang et al 26 attempted to resolve this controversy and listed the evidence of profibrotic function of miR-21. In in vivo studies, they found an increase in miR-21 and a decrease in TGF-β receptor III (TGF-β RIII) expression in the zone surrounding the area of myocardial infarction in the mouse heart.…”

Section: Mir-21mentioning

confidence: 99%

MicroRNAs Involved in the Regulation of Postischemic Cardiac Fibrosis

et al. 2013

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A novel reciprocal loop between microRNA-21 and TGFβRIII is involved in cardiac fibrosis

Cited by 148 publications

References 37 publications

Transforming Growth Factor‐β Receptor III is a Potential Regulator of Ischemia‐Induced Cardiomyocyte Apoptosis

Transforming Growth Factor‐β Receptor III is a Potential Regulator of Ischemia‐Induced Cardiomyocyte Apoptosis

MicroRNAs in myocardial ischemia: identifying new targets and tools for treating heart disease. New frontiers for miR-medicine

MicroRNAs Involved in the Regulation of Postischemic Cardiac Fibrosis

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