CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy

Yuan, Weiwei; Tang, Chengxiang; Zhu, Wenwei; Zhu, Ji-Xiao; Lin, Qiaoli; Fu, Yong-Heng; Deng, Chunyu; Xue, Yan; Wu, Shulin; Shan, Zhi

doi:10.1007/s11010-015-2635-4

Cited by 32 publications

(27 citation statements)

References 25 publications

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“…In the present study, miR-1, -133b and -16 were decreased, but miR-21 was increased in the fibrotic myocardium of a mouse Ang-II infusion model, which were consistent with previous reports [20–25]. Contrast to the previous reports that miR-214 was upregulated in the myocardium of a rat AAC model, and of a mouse ischemia/reperfusion (IR) injury model and of a rat isoproterenol injection model [16–19], our present data showed that miR-214-3p was significantly down-regulated in the myocardium of a mouse Ang-II infusion model, and was upregulated in Ang-II-induced mouse myofibroblasts.…”

Section: Discussionsupporting

confidence: 94%

“…According to our previous report [20], the recombinant luciferase reporter plasmid containing the potential miR-214-3p binding site sequences of EZH1 and -2 genes were constructed. Using a site-directed mutagenesis kit (TransGen, Beijing, China), the miR-214-3p binding site sequence CCUGCUG was replaced with CCACGAG, CCAGCUG was replaced with CCACGAG to construct the corresponding recombinant luciferase reporter plasmids containing the mutant potential miR-214 binding sequences.…”

Section: Methodsmentioning

confidence: 99%

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Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts

et al. 2016

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The role of microRNA-214-3p (miR-214-3p) in cardiac fibrosis was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced cardiac fibrosis. MiR-214-3p was markedly decreased in the fibrotic myocardium of a mouse Ang-II infusion model, but was upregulated in Ang-II-treated mouse myofibroblasts. Cardiac fibrosis was shown attenuated in Ang-II-infused mice received tail vein injection of miR-214-3p agomir. Consistently, miR-214-3p inhibited the expression of Col1a1 and Col3a1 in mouse myofibroblasts in vitro. MiR-214-3p could bind the 3′-UTRs of enhancer of zeste homolog 1 (EZH1) and −2, and suppressed EZH1 and −2 expressions at the transcriptional level. Functionally, miR-214-3p mimic, in parallel to EZH1 siRNA and EZH2 siRNA, could enhance peroxisome proliferator-activated receptor-γ (PPAR-γ) expression and inhibited the expression of Col1a1 and Col3a1 in myofibroblasts. In addition, enforced expression of EZH1 and −2, and knockdown of PPAR-γ resulted in the increase of Col1a1 and Col3a1 in myofibroblasts. Moreover, the NF-κB signal pathway was verified to mediate Ang-II-induced miR-214-3p expression in myofibroblasts. Taken together, our results revealed that EZH1 and −2 were novel targets of miR-214-3p, and miR-214-3p might be one potential miRNA for the prevention of cardiac fibrosis.

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Section: Discussionsupporting

confidence: 94%

Section: Methodsmentioning

confidence: 99%

Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts

et al. 2016

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“…As in our previous report27, the recombinant luciferase reporter plasmids containing the potential miR-26b-5p binding site sequences of the Col1a2 and CTGF genes were constructed. Human embryonic kidney (HEK) 293 cells (3 × 105 cells per well in 12-well plate) were co-transfected with 200 ng of recombinant luciferase reporter plasmid, 20 ng of pRL-TK as an internal control (Promega, Madison, WI), 200 ng of pDsRed2-N1 or 200 ng of pDsRed2-circRNA_000203, 50 nM miR-26b mimic or 50 nM mutant miR-26b mimic (the seed sequence of miR-26b UCAAGUA was changed with UGUUCUA), respectively.…”

Section: Methodsmentioning

confidence: 99%

CircRNA_000203 enhances the expression of fibrosis-associated genes by derepressing targets of miR-26b-5p, Col1a2 and CTGF, in cardiac fibroblasts

Tang

Zhang

Huang

et al. 2017

Sci Rep

234

168

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Circular RNAs (circRNAs) participate in regulating gene expression in diverse biological and pathological processes. The present study aimed to investigate the mechanism underlying the modulation of circRNA_000203 on expressions of fibrosis-associated genes in cardiac fibroblasts. CircRNA_000203 was shown upregulated in the diabetic mouse myocardium and in Ang-II-induced mouse cardiac fibroblasts. Enforced-expression of circRNA_000203 could increase expressions of Col1a2, Col3a1 and α-SMA in mouse cardiac fibroblasts. RNA pull-down and RT-qPCR assay indicated that circRNA_000203 could specifically sponge miR-26b-5p. Dual luciferase reporter assay revealed that miR-26b-5p interacted with 3′UTRs of Col1a2 and CTGF, and circ_000203 could block the interactions of miR-26b-5p and 3′UTRs of Col1a2 and CTGF. Transfection of miR-26b-5p could post-transcriptionaly inhibit expressions of Col1a2 and CTGF, accompanied with the suppressions of Col3a1 and α-SMA in cardiac fibroblasts. Additionally, over-expression of circRNA_000203 could eliminate the anti-fibrosis effect of miR-26b-5p in cardiac fibroblasts. Together, our results reveal that suppressing the function of miR-26b-5p contributes to the pro-fibrosis effect of circRNA_000203 in cardiac fibroblasts.

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“…In fact, miR‐1 has been consistently demonstrated to participate in diverse cardiovascular diseases, such as cardiac hypertrophy, arrhythmias and heart failure . Moreover, our previous study has shown up‐regulation of miR‐1 contributes to cardiac electrical remodelling induced by arsenic and atrioventricular block .…”

Section: Discussionmentioning

confidence: 58%

“…[10] Besides, tanshinone IIA relieved ischaemia-induced injury in postinfarction rat by inhibiting miR-1 expression through p38 MAPK signalling pathway. [28] In fact, miR-1 has been consistently demonstrated to participate in diverse cardiovascular diseases, such as cardiac hypertrophy, [29] arrhythmias [30] and heart failure. [31] Moreover, our previous study has shown up-regulation of miR-1 contributes to cardiac electrical remodelling induced by arsenic [32] and atrioventricular block.…”

Section: Discussionmentioning

confidence: 99%

Metoprolol protects against myocardial infarction by inhibiting miR-1 expression in rats

Qin

Zhang

et al. 2020

Journal of Pharmacy and Pharmacology

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Objectives Metoprolol is regarded as a first‐line medicine for the treatment of myocardial infarction (MI). However, the underlying mechanisms remain largely unknown. This study aimed to investigate the involvement of miR‐1 in the pharmacological function of metoprolol. Methods In vivo MI model was established by left anterior descending coronary artery (LAD) ligation. The effects of metoprolol on infarct size and cardiac dysfunction were determined by triphenyltetrazolium chloride staining and cardiac echocardiography, respectively. In vitro oxidative stress cardiomyocyte model was established by H2O2 treatment. The effect of metoprolol on the expression of miR‐1 and connexin43 (Cx43) was quantified by real‐time PCR and western blot, respectively. The intercellular communication was evaluated by lucifer yellow dye diffusion. Key findings Left anterior descending ligation‐induced MI injury was markedly attenuated by metoprolol as shown by reduced infarct size and better cardiac function. Metoprolol reversed the up‐regulation of miR‐1 and down‐regulation of Cx43 in MI heart. Moreover, in H2O2‐stimulated cardiomyocytes, overexpression of miR‐1 abolished the effects of metoprolol on Cx43 up‐regulation and increased intercellular communication, indicating that miR‐1 may be a necessary mediator for the cardiac protective function of metoprolol. Conclusions Metoprolol relieves MI injury via suppression miR‐1, thus increasing its target protein Cx43 and improving intercellular communication.

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CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy

Cited by 32 publications

References 25 publications

Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts

Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts

CircRNA_000203 enhances the expression of fibrosis-associated genes by derepressing targets of miR-26b-5p, Col1a2 and CTGF, in cardiac fibroblasts

Metoprolol protects against myocardial infarction by inhibiting miR-1 expression in rats

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