Down-regulation of miR-30b-5p protects cardiomyocytes against hypoxia-induced injury by targeting Aven

Zhang, Lanfang; Xinwei, Jia

doi:10.1186/s11658-019-0187-4

Cited by 19 publications

(12 citation statements)

References 29 publications

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“…Early report has proved that miR‐30b‐5p expression is significantly upregulated in hypoxic treated human cardiomyocyte line AC16 cells. Downregulation of miR‐30b‐5p effectively alleviated hypoxia‐induced cardiomyocyte injury and Aven is a potential target gene of miR‐30b‐5p and its downregulation could partially reverse the influence of miR‐30b‐5p knockdown on AC16 cells under hypoxia 23 . Herein, we validated that miR‐30a‐5p was remarkedly upregulated in H/R treated H9c2 cell and the heart tissue of rat following I/R.…”

Section: Discussionsupporting

confidence: 55%

Critical functions of microRNA‐30a‐5p‐E2F3 in cardiomyocyte apoptosis induced by hypoxia/reoxygenation

Niu

Zhang

et al. 2020

The Kaohsiung J of Med Scie

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The high‐mortality rate of cardiovascular diseases (CVDs) is associated with the myocardial ischemia and reperfusion (I/R). Recent investigations have revealed that microRNAs (miRNAs) exert vital functions in the apoptosis of cardiomyocyte cell. Nevertheless, the potential role of miR‐30a‐5p in the regulation of cardiomyocyte cell apoptosis needs to be illuminated. In the current study, we observed that hypoxia/reoxygenation (H/R) remarkably raised the level of miR‐30a‐5p but reduced the expression of E2F transcription factor 3 (E2F3) in H9c2 cardiomyocytes. In vivo, miR‐30a‐5p was found to be significantly upregulated in the hearts of rats following I/R. Downregulation of miR‐30a‐5p using anti‐miR‐30a‐5p decreased H9c2 cardiomyocytes apoptosis caused by H/R and promoted the proliferation of H9c2 inhibited by H/R. Moreover, E2F3 was a possible target gene of miR‐30a‐5p and upregulation of miR‐30a‐5p reduced the expression level of E2F3 in H9c2 cardiomyocytes. We further identified that E2F3 silencing reversed the effect of anti‐miR‐30a‐5p on the proliferation and apoptosis in H/R treated H9c2 cells. These studies suggested that downregulation of miR‐30a‐5p attenuated the impact of H/R on H9c2 cardiomyocytes through targeting E2F3.

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Section: Discussionsupporting

confidence: 55%

Critical functions of microRNA‐30a‐5p‐E2F3 in cardiomyocyte apoptosis induced by hypoxia/reoxygenation

Niu

Zhang

et al. 2020

The Kaohsiung J of Med Scie

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“…46 Inhibition of miR-30b-5p protected cardiomyocytes against hypoxia-induced injury by targeting Aven. 47 miR-30b-5p directly targeted the Scn8a 3 0 UTR and alleviated the oxaliplatin-induced chronic neuropathic pain by the negative regulation of the voltage-gated sodium channel Na v 1.6 expression in DRG neurons of rats. 48 What is more, miR-30b-5p agomir (mimic in vivo) was injected into liver injury mice via tail vein injection in the present study.…”

Section: Discussionmentioning

confidence: 98%

Cannabinoid Receptor 1/miR-30b-5p Axis Governs Macrophage NLRP3 Expression and Inflammasome Activation in Liver Inflammatory Disease

Yang

Tian

Zhang

et al. 2020

Molecular Therapy - Nucleic Acids

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Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) has been regarded as an important initiator or promoter in multiple inflammatory diseases. However, the relationship between cannabinoid receptor 1 (CB1) and macrophage NLRP3 inflammasome and the corresponding molecular mechanism in liver inflammation remain unclear. Mouse liver injury models were induced by carbon tetrachloride (CCl 4 ) or methionine-choline-deficient and high fat (MCDHF) diet. Human liver tissues were obtained from patients with different chronic liver diseases. CB1 expression was increased in liver tissue and macrophages of CCl 4 -and MCDHF-treated mice, positively correlated with NLRP3. CB1 agonist ACEA (Arachiodonyl-2'-Chloroethylamide) promoted NLRP3 expression and NLRP3 inflammasome activation in macrophages. CB1 blockade with its antagonist AM281 reduced NLRP3 expression, inflammasome activation, and liver inflammation in CCl 4 -and MCDHF-treated mice. MicroRNA-30b-5p (miR-30b-5p), screened by the intersection of bioinformatics databases and downregulated miRNAs in injured liver, negatively correlated with NLRP3 in mouse and human liver. miR-30b-5p was involved in CB1-mediated activation of NLRP3 inflammasome in macrophages by directly targeting NLRP3. Importantly, administration of miR-30b-5p agomir targeted NLRP3 and attenuated liver inflammation in the injured liver. Altogether, CB1/miR-30b-5p axis modulates NLRP3 expression and NLPR3 inflammasome activation in macrophages during liver inflammation, which provides a potential target for liver disease.

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“…Apoptosis and caspase activation inhibitor (AVEN) is an anti-apoptotic protein that controls apoptosis partially by abrogating caspase activation via binding to Bcl-xL and apoptotic peptidase activating factor (Apaf)-1. AVEN was demonstrated to mediate the protective effect of miR-30b-5p on hypoxia-induced cardiomyocyte injury ( 29 ).…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanism of CAIF inhibiting myocardial infarction by sponging miR‑488 and regulating AVEN expression

Li¹,

Chen²,

Wang³

et al. 2022

Mol Med Rep

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In recent years, the global incidence and mortality of myocardial infarction (MI) has increased and become one of the important diseases threatening public health. Long non-coding (lnc)RNAs are a type of ncRNA that serve critical roles in the progression of various types of disease. The present study aimed to investigate the effect and mechanism of lncRNA cardiac autophagy inhibitory factor (CAIF) on cardiac ischemia/reperfusion (I/R) injury. CAIF was downregulated in the myocardium of I/R rats and cardiomyocytes treated with hydrogen peroxide (H 2 O 2 ). Further experiments demonstrated that CAIF overexpression inhibited I/R-induced cardiac infarction and apoptosis in vivo . CAIF decreased H 2 O 2 -induced apoptosis and oxidative stress of cardiomyocytes. Mechanistically, CAIF sponged microRNA (miR)-488-5p; this interaction was confirmed by rescue experiments. Moreover, miR-488-5p targeted apoptosis and caspase activation inhibitor (AVEN) and inhibited its expression. In summary, the present data identified a novel CAIF/miR-488-5p/AVEN signaling axis as a key regulator of myocyte apoptosis, which may be a potential therapeutic target for the treatment of MI.

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Down-regulation of miR-30b-5p protects cardiomyocytes against hypoxia-induced injury by targeting Aven

Cited by 19 publications

References 29 publications

Critical functions of microRNA‐30a‐5p‐E2F3 in cardiomyocyte apoptosis induced by hypoxia/reoxygenation

Critical functions of microRNA‐30a‐5p‐E2F3 in cardiomyocyte apoptosis induced by hypoxia/reoxygenation

Cannabinoid Receptor 1/miR-30b-5p Axis Governs Macrophage NLRP3 Expression and Inflammasome Activation in Liver Inflammatory Disease

Molecular mechanism of CAIF inhibiting myocardial infarction by sponging miR‑488 and regulating AVEN expression

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