By Targeting Atg7 MicroRNA-143 Mediates Oxidative Stress-Induced Autophagy of c-Kit+ Mouse Cardiac Progenitor Cells

Ma, Wanbiao; Ding, Fengzhi; Wang, Xiuxiu; Huang, Qi; Zhang, Lai; Bi, Chongwei; Hua, Bingjie; Yuan, Ye; Han, Zhenbo; Jin, Mengyu; Liu, Tianyi; Yu, Ying; Cai, Benzhi; Du, Zhenhong

doi:10.1016/j.ebiom.2018.05.021

Cited by 28 publications

(20 citation statements)

References 26 publications

(29 reference statements)

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“…Acting as the only E1-like enzyme, Atg7 is located in the hub of the LC3 and Atg12 ubiquitin-like systems and is essential for the expansion of autophagosomal membranes [22]. Accumulating evidence suggests that Atg7 is not only a crucial marker of autophagy, but also participates in the regulation of cell death and survival [32,33], including in cardiac progenitor cells [34]. Previously, we noted that the expression of miR-27a-5p decreased in acute hypoxia-exposed H9c2 cells using a small RNA-seq, as a known hypoxamiR, however, its underlying function in the cardiomyocyte hypoxic response is unclear [13].…”

Section: Discussionmentioning

confidence: 99%

miR-27a-5p Attenuates Hypoxia-induced Rat Cardiomyocyte Injury by Inhibiting Atg7

Zhang

Qiu

et al. 2019

IJMS

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Acute myocardial infarction (AMI) is an ischemic heart disease with high mortality worldwide. AMI triggers a hypoxic microenvironment and induces extensive myocardial injury, including autophagy and apoptosis. MiRNAs, which are a class of posttranscriptional regulators, have been shown to be involved in the development of ischemic heart diseases. We have previously reported that hypoxia significantly alters the miRNA transcriptome in rat cardiomyoblast cells (H9c2), including miR-27a-5p. In the present study, we further investigated the potential function of miR-27a-5p in the cardiomyocyte response to hypoxia, and showed that miR-27a-5p expression was downregulated in the H9c2 cells at different hypoxia-exposed timepoints and the myocardium of a rat AMI model. Follow-up experiments revealed that miR-27a-5p attenuated hypoxia-induced cardiomyocyte injury by regulating autophagy and apoptosis via Atg7, which partly elucidated the anti-hypoxic injury effects of miR-27a-5p. Taken together, this study shows that miR-27a-5p has a cardioprotective effect on hypoxia-induced H9c2 cell injury, suggesting it may be a novel target for the treatment of hypoxia-related heart diseases.

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Section: Discussionmentioning

confidence: 99%

miR-27a-5p Attenuates Hypoxia-induced Rat Cardiomyocyte Injury by Inhibiting Atg7

Zhang

Qiu

et al. 2019

IJMS

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“…Moreover, they found that the silencing of miR-143 upregulates Atg7 expression and promotes the autophagy of c-kit + cardiac progenitor cells (CPCs) exposed to H 2 O 2 . 34 Moreover, the transplantation of c-kit + CPCs with miR-143 inhibitor improves cell survival and enhanced therapeutic efficiency in MI. 34 …”

Section: Main Textmentioning

confidence: 99%

“… 34 Moreover, the transplantation of c-kit + CPCs with miR-143 inhibitor improves cell survival and enhanced therapeutic efficiency in MI. 34 …”

Section: Main Textmentioning

confidence: 99%

Autophagy in cardiovascular diseases: role of noncoding RNAs

Gao

Chen

Shan

et al. 2021

Molecular Therapy - Nucleic Acids

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Cardiovascular diseases (CVDs) remain the world’s leading cause of death. Cardiomyocyte autophagy helps maintain normal metabolism and functioning of the heart. Importantly, mounting evidence has revealed that autophagy plays a dual role in CVD pathology. Under physiological conditions, moderate autophagy maintains cell metabolic balance by degrading and recycling damaged organelles and proteins, and it promotes myocardial survival, but excessive or insufficient autophagy is equally deleterious and contributes to disease progression. Noncoding RNAs (ncRNAs) are a class of RNAs transcribed from the genome, but most ncRNAs do not code for functional proteins. In recent years, increasingly, various ncRNAs have been identified, and they play important regulatory roles in the physiological and pathological processes of organisms, as well as in autophagy. Thus, determining whether ncRNA-regulated autophagy plays a protective role in CVDs or promotes their progression can help us to develop ncRNAs as therapeutic targets in autophagy-related CVDs. In this review, we briefly summarize the regulatory roles of several important ncRNAs, including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), in the autophagy of various CVDs to provide a theoretical basis for the etiology and pathogenesis of CVDs and develop novel therapies to treat CVDs.

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“…Previous studies have observed autophagy activation in ectopic endometrium of patients with ovarian endometriosis ( 17 , 25 , 26 ). Based on the finding that miR-143-3p displays the potential to regulate autophagy in other diseases ( 27 , 28 ), the present study investigated whether miR-143-3p inhibited ESC proliferation and invasion via inactivating autophagy. The activation of autophagy was analyzed using an autophagy detection kit and western blotting.…”

Section: Resultsmentioning

confidence: 99%

miR‑143‑3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis

Yang

Hang

et al. 2021

Mol Med Rep

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Endometriosis (EM) is a multifactorial and debilitating chronic benign gynecological disease, but the pathogenesis of the disease is not completely understood. Dysregulated expression of microRNAs (miRNA/miR) is associated with the etiology of EM due to their role in regulating endometrial stromal cell proliferation and invasion. The present study aimed to identify the functions and mechanisms underlying miR-143-3p in EM. To explore the role of miR-143-3p in EM, functional miRNAs were analyzed via bioinformatics analysis. miR-143-3p expression levels in endometriotic stromal cells (ESCs) and normal endometrial stromal cells (NESCs) were measured via reverse transcription-quantitative PCR. The role of miR-143-3p in regulating ESC proliferation and invasion was assessed by performing Cell Counting Kit-8 and Transwell assays, respectively. miR-143-3p expression was significantly upregulated in ESCs compared with NESCs. Functionally, miR-143-3p overexpression inhibited ESC proliferation and invasion, whereas miR-143-3p knockdown promoted ESC proliferation and invasion. Moreover, miR-143-3p inhibited autophagy activation in ESCs, as indicated by decreased green puncta, which represented autophagic vacuoles, decreased microtubule associated protein 1 light chain 3α expression and increased p62 expression in the miR-143-4p mimic group compared with the control group. Moreover, compared with the control group, miR-143-3p overexpression significantly decreased the expression levels of autophagy-related 2B (ATG2B), a newly identified target gene of miR-143-3p, in ESCs. ATG2B overexpression reversed miR-143-3p overexpression-mediated inhibition of ESC proliferation and invasion. Collectively, the results of the present study suggested that miR-143-3p inhibited EM progression, thus providing a novel target for the development of therapeutic agents against EM.

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By Targeting Atg7 MicroRNA-143 Mediates Oxidative Stress-Induced Autophagy of c-Kit+ Mouse Cardiac Progenitor Cells

Cited by 28 publications

References 26 publications

miR-27a-5p Attenuates Hypoxia-induced Rat Cardiomyocyte Injury by Inhibiting Atg7

miR-27a-5p Attenuates Hypoxia-induced Rat Cardiomyocyte Injury by Inhibiting Atg7

Autophagy in cardiovascular diseases: role of noncoding RNAs

miR‑143‑3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis

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