Aberrant expression of miR‐29b‐3p influences heart development and cardiomyocyte proliferation by targeting NOTCH2

Yang, Qian; Wu, Fang; Mi, Yaping; Wang, Feng; Cai, Ke; Yang, Xianghua; Zhang, Ranran; Liu, Lian; Zhang, Yawen; Wang, Youhua; Wang, Xu; Xu, Mingqing; Gui, Yonghao; Li, Qiang

doi:10.1111/cpr.12764

Cited by 48 publications

(36 citation statements)

References 59 publications

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“…Besides, H19 has been identi ed as a regulator that targets PPARα of cardiac hypertrophy [25,26]. The results showed that XIST, MALAT1 and H19 possibly regulated other miRNAs involved in cardiac hypertrophy, such as miR-15b [27], miR-19b [28] and miR-29b [29] in our research.…”

Section: Discussionsupporting

confidence: 55%

Analysis of multi-factor regulated network and different clusters in hypertrophic obstructive cardiomyopathy

Huang¹,

Chen²,

Wen³

et al. 2021

Preprint

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We herein explored the regulatory network between lncRNA, miRNAs, mRNAs, and TFs in the HOCM and divided HOCM samples into different clusters to identify key genes and regulatory factors. The four gene sets from GEO, GENE and OMIM databases were integrated and WGCNA network was used to obtain two modules and 32 core genes. Through online database, miRNA-lncRNA, miRNA-mRNA, and TF-mRNA interaction pairs were obtained to screen the regulatory factors, and finally a multi-factor regulatory network was obtained. The first 7 regulatory factors were obtained as the core regulatory factors. The unsupervised clustering method was used to divide HOCM samples into 4 clusters. As a result, four genes including COMP, FMOD, AEBP1 and SULF1 showed significant expression in different clusters. Finally, we got 4 genes are considered as important biomarkers for different progressive stages or prognosis of HOCM. These might assist in discovering molecular mechanisms of HOCM in the future.

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Section: Discussionsupporting

confidence: 55%

Analysis of multi-factor regulated network and different clusters in hypertrophic obstructive cardiomyopathy

Huang¹,

Chen²,

Wen³

et al. 2021

Preprint

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show abstract

“…Besides, H19 has been identi ed as a regulator that targets PPARα of cardiac hypertrophy (Liu et al, 2016;Zhou et al, 2019). The results showed that XIST, MALAT1 and H19 possibly regulated other miRNAs involved in cardiac hypertrophy, such as miR-15b (Ooi et al, 2014), miR-19b (Li et al, 2019) and miR-29b (Yang et al, 2020) in our research.…”

Section: Discussionsupporting

confidence: 55%

Analysis of multi-factor regulated network and different clusters in hypertrophic obstructive cardiomyopathy

Huang

Chen

Wen

et al. 2020

Preprint

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Background Hypertrophic obstructive cardiomyopathy (HOCM) is a kind of hypertrophic cardiomyopathy (HCM) with more severe symptoms. We herein explored the regulatory network between lncRNA, miRNAs, mRNAs, and TFs in the HOCM and divided HOCM samples into different clusters to identify key genes and regulatory factors that are involved in the process of HOCM. Methods Differentially expressed genes and online associated genes were integrated as a candidate gene set. WGCNA method was used to obtain key modules and genes related to HOCM. Subsequently, core genes were used to construct a multi-factor regulatory network and divided HOCM into different clusters. Lastly, the key regulatory factors and significant genes were identified in different clusters. Results The four gene sets from GEO, GENE and OMIM databases were integrated and WGCNA network was used to obtain two modules and 32 core genes. Through online database, miRNA-lncRNA, miRNA-mRNA, and TF-mRNA interaction pairs were obtained to screen the regulatory factors that interact with the co-expressed key genes (N = 32), and finally a multi-factor regulatory network with 175 interaction pairs was obtained. The first 7 regulatory factors were obtained as the core regulatory factors, which included the lncRNAs (XIST, MALAT1, H19), TFs (SPI1 and SP1) and miRNAs (hsa-miR-29b-39 and has-miR-29a-3p). Finally, the unsupervised clustering method was used to divide HOCM samples into 4 clusters. As a result, four genes including COMP, FMOD, AEBP1 and SULF1 showed significant expression in different clusters. Conclusion Bioinformatics method was used to obtain the molecular regulatory lncRNA-miRNA-mRNA and TF network and classified HOCM samples into different clusters. Finally, 32 co-expressed key genes that are of great significance for HOCM typing and 4 genes are considered as important biomarkers for different progressive stages or prognosis of HOCM. These might assist in discovering molecular mechanisms of HOCM in the future.

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“…Increasing evidence suggests that abnormal expression miR-29a-3p is in association with various heart diseases. For example, its expression is upregulated in the right ventricular outflow tract of congenital heart disease patients [ 16 ]. Moreover, it suppresses cardiomyocyte proliferation.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-29a-3p Suppresses Proliferation, Migration, and Invasion of Vascular Smooth Muscle Cells in Atherosclerosis via Targeting TNFRSF1A

You

Chen

et al. 2020

BioMed Research International

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Objective. Increasing evidence highlights the significance of microRNAs (miRNAs) in the progression of atherosclerosis (AS). Our aim was to probe out the role and regulatory mechanism of miR-29a-3p in AS. Methods. An in vivo model of AS was conducted by high-fat diet ApoE-/- mice. Oxidized low-density lipoprotein- (ox-LDL-) exposed vascular smooth muscle cells (VSMCs) were utilized as an in vitro of AS. Serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were detected. Hematoxylin and eosin (H&E) and Masson’s staining was presented to investigate the pathological changes. miR-29a-3p and TNFRSF1A expression was detected by RT-qPCR. Proliferative, migrated, and invaded abilities of VSMCs were determined via a series of assays. The interaction between miR-29a-3p and TNFRSF1A was verified through luciferase reporter assay. Results. Upregulated miR-29a-3p and downregulated TNFRSF1A were found both in vitro and in vivo models of AS. miR-29a-3p mimic distinctly decreased the serum levels of TC, TG, and LDL-C and increased serum HDL-C levels. Moreover, its overexpression could ameliorate plaque formation of AS mice. In ox-LDL-induced VSMCs, miR-29a-3p overexpression notably decreased cell proliferation, migration, and invasion, which was reversed by TNFRSF1A overexpression. Also, miR-29a-3p could directly target the 3′UTR of TNFRSF1A. Conclusion. miR-29a-3p overexpression ameliorated plaque formation of AS and suppressed proliferation, migration, and invasion of ox-LDL-induced VSMCs via TNFRSF1A, which offered novel insights into the progression of AS.

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Aberrant expression of miR‐29b‐3p influences heart development and cardiomyocyte proliferation by targeting NOTCH2

Cited by 48 publications

References 59 publications

Analysis of multi-factor regulated network and different clusters in hypertrophic obstructive cardiomyopathy

Analysis of multi-factor regulated network and different clusters in hypertrophic obstructive cardiomyopathy

Analysis of multi-factor regulated network and different clusters in hypertrophic obstructive cardiomyopathy

Overexpression of miR-29a-3p Suppresses Proliferation, Migration, and Invasion of Vascular Smooth Muscle Cells in Atherosclerosis via Targeting TNFRSF1A

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