Effects of miR-23b on hypoxia-induced cardiomyocytes apoptosis

He, Weilai; Chen, Hong; Jin, Chaolong; Ge, Shuping

doi:10.1016/j.biopha.2017.09.148

Cited by 18 publications

(6 citation statements)

References 25 publications

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“…An intervention to determine if beneficial effects can be achieved by manipulation of the intestinal microbiota to reduce systemic inflammation, as has been observed after critical illness ( 60 , 61 ), is required in this patient population. Additionally, recent findings support the involvement of micro–ribonucleic acid in both the development and exacerbation of CHD as well as influences on the microbiome ( 62 , 63 , 64 , 65 , 66 ). Targeting micro–ribonucleic acid may also yield therapeutic interventions.…”

Section: Discussionmentioning

confidence: 63%

Dysbiosis and Intestinal Barrier Dysfunction in Pediatric Congenital Heart Disease Is Exacerbated Following Cardiopulmonary Bypass

Salomon

Ericsson

Price

et al. 2021

JACC: Basic to Translational Science

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Section: Discussionmentioning

confidence: 63%

Dysbiosis and Intestinal Barrier Dysfunction in Pediatric Congenital Heart Disease Is Exacerbated Following Cardiopulmonary Bypass

Salomon

Ericsson

Price

et al. 2021

JACC: Basic to Translational Science

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“…Both microR-129-5p and miR-19b have been identified as a biomarker for heart failure and diabetic cardiomyopathy respectively, as suggested by the literature and this was further validated by inducting hypoxia to their respective cell culture models 26,27 . Similarly, hypoxia gradually increases miR-23b in cardiomyocyte and prevented the growth by apoptosis 28 . Among the two gene families, DNMT3A and HIF1A showed maximum cardiovascular diseases related targets in Table 1, searched via TargetScan database.…”

Section: Discussionmentioning

confidence: 99%

micro-RNAs dependent regulation of DNMT and HIF1α gene expression in thrombotic disorders

Vijay

Jha

Garg

et al. 2019

Sci Rep

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MicroRNAs (miRNAs) are involved in a wide variety of cellular processes and post-transcriptionally regulate several mechanism and diseases. However, contribution of miRNAs functioning during hypoxia and DNA methylation together is less understood. The current study was aimed to find a shared miRNAs signature upstream to hypoxia (via HIF gene family members) and methylation (via DNMT gene family members). This was followed by the global validation of the hypoxia related miRNA signature using miRNA microarray meta-analysis of the hypoxia induced human samples. We further concluded the study by looking into thrombosis related terms and pathways enriched during protein-protein interaction (PPI) network analysis of these two sets of gene family. Network prioritization of these shared miRNAs reveals miR-129, miR-19band miR-23b as top regulatory miRNAs. A comprehensive meta-analysis of microarray datasets of hypoxia samples revealed 29 differentially expressed miRNAs. GSEA of the interacting genes in the DNMT-HIF PPI network indicated thrombosis associated pathways including “Hemostasis”, “TPO signaling pathway” and “angiogenesis”. Interestingly, the study has generated a novel database of candidate miRNA signatures shared between hypoxia and methylation, and their relation to thrombotic pathways, which might aid in the development of potential therapeutic biomarkers.

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“…A previous study demonstrated that downregulation of miR-23b increased Smad3 protein expression levels, which facilitated the proliferation of heat-denatured fibroblasts (34). Furthermore, a number of other studies have suggested that Smad3 is the target gene of miR-23b-3p in rat fibroblasts and other cells (34–39); thus, it was hypothesized that miR-23b-3p may induce human fibroblast apoptosis by targeting Smad3. The exact effects of miR-23b-3p on fibroblast apoptosis requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

10‑Hydroxycamptothecin induces apoptosis in human fibroblasts by regulating miRNA‑23b‑3p expression

Zeng

Sun

et al. 2019

Mol Med Report

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10-Hydroxycamptothecin (HCPT) effectively controls epidural fibrosis, but the exact underlying mechanisms remain ambiguous. Abnormal microRNA (miR)-23b-3p expression has been detected in various types of fibrotic tissues that are present in different diseases. The aim of the present study was to elucidate the mechanisms through which HCPT induces fibroblast apoptosis. Reverse transcription-quantitative polymerase chain reactions were performed on six traumatic scar samples and matched normal skin samples; traumatic scar formation was revealed to be significantly inversely associated with miR-23b-3p expression. In addition, the miR-23b-3p expression level in human fibroblasts was examined following HCPT treatment. The effects of HCPT and miR-23b-3p on fibroblast apoptosis were assessed using terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling, flow cytometry and western blot analysis. The results demonstrated that HCPT treatment notably increased miR-23b-3p expression levels and accelerated fibroblast apoptosis. Therefore, upregulation of miR-23b-3p expression was demonstrated to promote fibroblast apoptosis, consistently with the effects of HCPT. The results of the present study indicated that HCPT may induce fibroblast apoptosis by regulating miR-23b-3p expression.

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Effects of miR-23b on hypoxia-induced cardiomyocytes apoptosis

Cited by 18 publications

References 25 publications

Dysbiosis and Intestinal Barrier Dysfunction in Pediatric Congenital Heart Disease Is Exacerbated Following Cardiopulmonary Bypass

Dysbiosis and Intestinal Barrier Dysfunction in Pediatric Congenital Heart Disease Is Exacerbated Following Cardiopulmonary Bypass

micro-RNAs dependent regulation of DNMT and HIF1α gene expression in thrombotic disorders

10‑Hydroxycamptothecin induces apoptosis in human fibroblasts by regulating miRNA‑23b‑3p expression

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