MicroRNAs Involved in the Regulation of Postischemic Cardiac Fibrosis

Dai, Yao; Khaidakov, Magomed; Wang, Xianwei; Ding, Zufeng; Su, Wei; Price, Elvin; Palade, Philip; Chen, Mingwei; Mehta, Jawahar L.

doi:10.1161/hypertensionaha.111.00654

Cited by 31 publications

(17 citation statements)

References 59 publications

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“…This is not a unique case as miRNA exerts biological effects in a cell‐specific manner . For example, miR‐21 inhibition has been reported to be able to reduce cardiac fibrosis, while it (miR‐21 inhibition) may also enhance cardiomyocyte hypertrophy . Besides that, similar phenomenon has been observed with miR‐24 and miR‐15 .…”

Section: Discussionmentioning

confidence: 86%

“…Dysregulation of miRNAs has already been linked to a large number of cardiovascular diseases including cardiac fibrosis [5,19]. Let-7, miR-21, miR-22, miR-34a, miR-208a, miR-377 and miR-652 have been reported to promote the genesis of cardiac fibrosis, while miR-1, miR-15 family, miR-24, miR-26a, miR-29b, miR-101, miR-122, miR-133, miR-145, miR-378 and miR-489 attenuate the fibrotic response of heart [6,20,21]. These reports suggest miRNA as powerful regulators of cardiac fibrosis [6,20,21].…”

Section: Introductionmentioning

confidence: 99%

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miR‐19b controls cardiac fibroblast proliferation and migration

Zhong

Wang

Liu

et al. 2016

J Cellular Molecular Medi

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Cardiac fibrosis is a fundamental constituent of a variety of cardiac dysfunction, making it a leading cause of death worldwide. However, no effective treatment for cardiac fibrosis is available. Therefore, novel therapeutics for cardiac fibrosis are highly needed. Recently, miR‐19b has been found to be able to protect hydrogen peroxide (H2O2)‐induced apoptosis and improve cell survival in H9C2 cardiomyocytes, while down‐regulation of miR‐19b had opposite effects, indicating that increasing miR‐19b may be a new therapeutic strategy for attenuating cellular apoptosis during myocardial ischaemia–reperfusion injury. However, considering the fact that microRNAs might exert a cell‐specific role, it is highly interesting to determine the role of miR‐19b in cardiac fibroblasts. Here, we found that miR‐19b was able to promote cardiac fibroblast proliferation and migration. However, miR‐19b mimics and inhibitors did not modulate the expression level of collagen I. Pten was identified as a target gene of miR‐19b, which was responsible for the effect of miR‐19b in controlling cardiac fibroblast proliferation and migration. Our data suggest that the role of miR‐19b is cell specific, and systemic miR‐19b targeting in cardiac remodelling might be problematic. Therefore, it is highly needed and also urgent to investigate the role of miR‐19b in cardiac remodelling in vivo.

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Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

miR‐19b controls cardiac fibroblast proliferation and migration

Zhong

Wang

Liu

et al. 2016

J Cellular Molecular Medi

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“…Data represent average of 2 blinded observers and graphed as mean + standard error of the mean (SEM). *P < .05, **P < .01, ***P < .001. changes in histone acetylation/deacetylation [23][24][25] and differential expression of microRNAs [26][27][28] in the pathogenesis of cardiac disease.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Therapy for the Treatment of Hypertension-Induced Cardiac Hypertrophy and Fibrosis

Watson

Horgan

Neary

et al. 2015

J Cardiovasc Pharmacol Ther

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“…Therefore it is one of the major biological determinants for fatal issues in cardiovascular diseases [2]. Methods for cardiac fibrosis inhibition are rare except for some anti-hypertensive drugs [3], inhibitors of matrix matalloproteinases [4], microRNAs intervention therapies [5], and stem cell transplantations etc [6], however their effects are not satisfactory.…”

Section: Introductionmentioning

confidence: 99%

Prostacyclin Analogue Beraprost Inhibits Cardiac Fibroblast Proliferation Depending on Prostacyclin Receptor Activation through a TGF β-Smad Signal Pathway

et al. 2014

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Previous studies showed that prostacyclin inhibited fibrosis. However, both receptors of prostacyclin, prostacyclin receptor (IP) and peroxisome proliferator-activated receptor (PPAR), are abundant in cardiac fibroblasts. Here we investigated which receptor was vital in the anti-fibrosis effect of prostacyclin. In addition, the possible mechanism involved in protective effects of prostacyclin against cardiac fibrosis was also studied. We found that beraprost, a prostacyclin analogue, inhibited angiotensin II (Ang II)-induced neonatal rat cardiac fibroblast proliferation in a concentration-dependent and time-dependent manner. Beraprost also suppressed Ang II-induced collagen I mRNA expression and protein synthesis in cardiac fibroblasts. After IP expression was knocked down by siRNA, Ang II-induced proliferation and collagen I synthesis could no longer be rescued by beraprost. However, treating cells with different specific inhibitors of PPAR subtypes prior to beraprost and Ang II stimulation, all of the above attenuating effects of beraprost were still available. Moreover, beraprost significantly blocked transforming growth factor β (TGF β) expression as well as Smad2 phosphorylation and reduced Smad-DNA binding activity. Beraprost also increased phosphorylation of cAMP response element binding protein (CREB) at Ser133 in the nucleus. Co-immunoprecipitation analysis revealed that beraprost increased CREB but decreased Smad2 binding to CREB-binding protein (CBP) in nucleus. In conclusion, beraprost inhibits cardiac fibroblast proliferation by activating IP and suppressing TGF β-Smad signal pathway.

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MicroRNAs Involved in the Regulation of Postischemic Cardiac Fibrosis

Cited by 31 publications

References 59 publications

miR‐19b controls cardiac fibroblast proliferation and migration

miR‐19b controls cardiac fibroblast proliferation and migration

Epigenetic Therapy for the Treatment of Hypertension-Induced Cardiac Hypertrophy and Fibrosis

Prostacyclin Analogue Beraprost Inhibits Cardiac Fibroblast Proliferation Depending on Prostacyclin Receptor Activation through a TGF β-Smad Signal Pathway

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