Profiling of miR-205/P4HA3 Following Angiotensin II-Induced Atrial Fibrosis: Implications for Atrial Fibrillation

Xiao, Zezhou; Reddy, Desai Pavan Kumar; Xue, Chuqing; Liu, Ximao; Chen, Xiong; Li, Jiale; Xiao, Langtao; Zheng, Shaoyi

doi:10.3389/fcvm.2021.609300

Cited by 17 publications

(12 citation statements)

References 32 publications

(31 reference statements)

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“…Evidence has shown that miR-205 is poorly expressed in angiotensin II-induced rat atrial fibrosis models [ 18 ]. Meanwhile, there were significant increases in EHMT2 expression and H3K9 methylation levels in TGF-β1-induced renal fibrosis mice and bleomycin-induced pulmonary fibrosis mice [ 20 , 37 ].…”

Section: Resultsmentioning

confidence: 99%

“…Investigations on these miRNAs shed light on the molecular mechanisms in the etiopathogenesis of AF and suggest miRNA targeting to be an appealing strategy for the treatment and management of this disorder [ 17 ]. Among these miRNAs, miR-205 has been recently illustrated to affect the progression of AF by regulating the functions of rat fibroblasts [ 18 ]. Meanwhile, miR-205-5p can act as an inhibitor of oxidative stress and inflammation in hypoxia/reoxygenation-injured rat hippocampal neurons [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-205-5p plays a suppressive role in the high-fat diet-induced atrial fibrosis through regulation of the EHMT2/IGFBP3 axis

et al. 2022

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Objective MicroRNAs (miRNAs) targeting has been revealed to be an appealing strategy for the treatment and management of atrial fibrillation (AF). In this research, we aimed to explore the mechanisms of miR-205-5p in reducing the high-fat diet (HFD)-induced atrial fibrosis through the EHMT2/IGFBP3 axis. Methods Expression levels of miR-205-5p, IGFBP3 and EHMT2 were determined in AF patients, cell fibrosis models and mouse atrial fibrosis models. Luciferase activity and RIP assays were performed to detect the binding between miR-205-5p and EHMT2, and ChIP assays were implemented to detect the enrichment of H3K9me2 and H3K4me3 in the promoter region of IGFBP3 in cells. The related experiments focusing on the inflammatory response, atrial fibrosis, mitochondrial damage, and metabolic abnormalities were performed to figure out the roles of miR-205-5p, IGFBP3, and EHMT2 in cell and mouse atrial fibrosis models. Results Low expression levels of miR-205-5p and IGFBP3 and a high expression of EHMT2 were found in AF patients, cell fibrosis models and mouse atrial fibrosis models. Upregulation of miR-205-5p reduced the expression of TGF-β1, α-SMA, Col III and other fibrosis-related proteins. miR-205-5p overexpression targeted EHMT2 to regulate the methylation of H3 histones to promote IGFBP3 expression, which in turn affected the fibrosis of atrial muscle cells. In HFD-induced atrial fibrosis mice, upregulated miR-205-5p or elevated IGFBP3 alleviated atrial fibrosis, mitochondrial damage, and metabolic abnormalities. Conclusion This study suggests that miR-205-5p attenuates HFD-induced atrial fibrosis via modulating the EHMT2/IGFBP3 axis. Graphical Abstract miR-205-5p alleviates high-fat diet-induced atrial fibrosis in mice via EHMT2/IGFBP3.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-205-5p plays a suppressive role in the high-fat diet-induced atrial fibrosis through regulation of the EHMT2/IGFBP3 axis

et al. 2022

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“…Furthermore, microRNA-181a has been demonstrated as an anti-fibrotic factor in fBMFs [ 54 ], and participated in TGF-β-induced EMT in hepatocytes [ 55 ]. As for miR-205, it was found to attenuate the angiotensin II-induced fibrosis in vivo and myofibroblast activation in atrial fibroblasts [ 56 ]. Given that we observed the decreased myofibroblast activities and TGF-β/Smad2 signaling in fBMFs with sh-lincROR, whether lincROR contributes to the development of OSF via functioning as a competing endogenous RNA of microRNA-145, microRNA-181, or miR-205 requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

α-Mangostin Inhibits the Activation of Myofibroblasts via Downregulation of Linc-ROR-Mediated TGFB1/Smad Signaling

et al. 2023

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Oral submucous fibrosis (OSF) is a premalignant disorder and persistent activation of myofibroblasts is implicated in this pathological progression. Increasing attention has been addressed towards non-coding RNA-regulated myofibroblasts activities and the effects of phytochemicals on non-coding RNA modulation are of great importance. In the present study, we examined the anti-fibrosis property of α-mangostin, a xanthone isolated from the pericarp of mangosteen. We found that α-mangostin exhibited inhibitory potency in myofibroblast activities and expression of fibrosis markers at the concentrations that caused neglectable damage to normal cells. Apart from the downregulation of TGF-β1/Smad2 signaling, we found that α-mangostin attenuated the expression of long non-coding RNA LincROR as well. Our results demonstrated that the effects of α-mangostin on myofibroblast activation were reverted when LincROR was overexpressed. Additionally, we showed the expression of LincROR in OSF specimens was elevated and silencing of LincROR successfully attenuated myofibroblast characteristics and TGF-β1/Smad2 activation. Taken together, these findings indicated that the anti-fibrosis effects of α-mangostin merit consideration and may be due to the attenuation of LincROR.

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“…egy to prevent or treat atrial fibrosis or AF in DCM. Reducing miR-205 expression in AF rats attenuated atrial fibrosis by targeting prolyl-hydroxylase α polypeptide III (P4Hα3) to inhibit CF proliferation and migration and inactivating the JNK pathway [29]. Other miRNAs are also involved in atrial remodeling, including miR-133, miR-590 and miR-146b-5p, and all were downregulated in a canine model of AF [30,44].…”

Section: Atrial Fibrosismentioning

confidence: 99%

Noncoding RNAs and Cardiac Fibrosis

Wu¹,

Bao²,

Li³

et al. 2023

Rev. Cardiovasc. Med.

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Myocardial fibrosis is a common pathological feature of various terminal cardiovascular diseases. Progressive fibrosis is the pathological basis for the development and progression of many cardiac arrhythmias and heart failure. There are no effective reversal drugs for myocardial fibrosis due to the lack of understanding of the molecular mechanisms. Noncoding RNAs, a class of RNAs that do not function in coding proteins, have been found to be intimately involved in the life cycle of cardiomyocyte differentiation, transcription and apoptosis and are important regulators of cardiovascular disease. An increasing number of studies have shown that noncoding RNAs regulate the proliferation and transformation of cardiac fibroblasts through related signaling pathways and can be used as potential biomarkers and novel therapeutic targets for cardiac fibrosis. This article reviews the relationship between noncoding RNAs and cardiac fibrosis.

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Profiling of miR-205/P4HA3 Following Angiotensin II-Induced Atrial Fibrosis: Implications for Atrial Fibrillation

Cited by 17 publications

References 32 publications

MicroRNA-205-5p plays a suppressive role in the high-fat diet-induced atrial fibrosis through regulation of the EHMT2/IGFBP3 axis

MicroRNA-205-5p plays a suppressive role in the high-fat diet-induced atrial fibrosis through regulation of the EHMT2/IGFBP3 axis

α-Mangostin Inhibits the Activation of Myofibroblasts via Downregulation of Linc-ROR-Mediated TGFB1/Smad Signaling

Noncoding RNAs and Cardiac Fibrosis

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