MiR-320 regulates cardiomyocyte apoptosis induced by ischemia–reperfusion injury by targeting AKIP1

Tian, Zhiqiang; Jiang, Hong; Lu, Zhibing

doi:10.1186/s11658-018-0105-1

Cited by 45 publications

(38 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miR-320 is presumably upregulated in the heart by hyperglycaemia, which acts through CD36 (fatty acid translocase) transcription [53]. Other studies determined that miR-320 overexpression is linked to cell death and apoptosis through heat-shock protein 20 [50] and insulin growth factor-1 [54], or by targeting AKIP1 and inducing the mitochondrial apoptotic pathway [55], among other mechanisms. Our results from in silico and computational miRNA target prediction algorithms revealed that miR-320a can regulate the expression of genes implicated in cardiac signalling pathways activated under ischaemia.…”

Section: Discussionmentioning

confidence: 99%

Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Galeano-Otero

Guisado

Díaz

et al. 2020

JCM

View full text Add to dashboard Cite

Restoration of epicardial coronary blood flow, achieved by early reperfusion with primary percutaneous coronary intervention (PPCI), is the guideline recommended to treat patients with ST-segment-elevation myocardial infarction (STEMI). However, despite successful blood restoration, increasing numbers of patients develop left ventricular adverse remodelling (LVAR) and heart failure. Therefore, reliable prognostic biomarkers for LVAR in STEMI are urgently needed. Our aim was to investigate the role of circulating microRNAs (miRNAs) and their association with LVAR in STEMI patients following the PPCI procedure. We analysed the expression of circulating miRNAs in blood samples of 56 patients collected at admission and after revascularization (at 3, 6, 12 and 24 h). The associations between miRNAs and left ventricular end diastolic volumes at 6 months were estimated to detect LVAR. miRNAs were also analysed in samples isolated from peripheral blood mononuclear cells (PBMCs) and human myocardium of failing hearts. Kinetic analysis of miRNAs showed a fast time-dependent increase in miR-133a, miR-133b, miR-193b, miR-499, and miR-320a in STEMI patients compared to controls. Moreover, the expression of miR-29a, miR-29b, miR-324, miR-208, miR-423, miR-522, and miR-545 was differentially expressed even before PPCI in STEMI. Furthermore, the increase in circulating miR-320a and the decrease in its expression in PBMCs were significantly associated with LVAR and correlated with the expression of miR-320a in human failing myocardium from ischaemic origin. In conclusion, we determined the time course expression of new circulating miRNAs in patients with STEMI treated with PPCI and we showed that miR-320a was positively associated with LVAR.

show abstract

Section: Discussionmentioning

confidence: 99%

Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Galeano-Otero

Guisado

Díaz

et al. 2020

JCM

View full text Add to dashboard Cite

show abstract

“…The induction of cardiomyocyte apoptosis is a rare event in the healthy myocardium and is the predominant form of cell death in the infarcted myocardium, which is often caused by ischemia (31,32). It has been shown that miRNAs are associated with the induction of cardiomyocyte apoptosis following ischemic injury (33).…”

Section: Discussionmentioning

confidence: 99%

Effects of miR‑103a‑3p on the autophagy and apoptosis of cardiomyocytes by regulating Atg5

Zhang

Wang

et al. 2019

Int J Mol Med

View full text Add to dashboard Cite

Autophagy and apoptosis are associated with cardiovascular diseases. Emerging evidence shows that microRNAs (miRs) are critical in the development of pathological processes underlying cardiovascular diseases by regulating the induction of apoptosis and autophagy. The present study aimed to investigate the role of miR-103a-3p in cardiomyocyte injury through autophagy and apoptosis. H9c2 cells were cultured under hypoxia and reoxygenation (H/R) conditions and were used to mimic cells under ischemia. The transfection of cells with miR-103a-3p (mimics and inhibitors) was performed to examine its function in cardiomyocytes. The expression levels of miR-103a-3p were evaluated by reverse transcription-quantitative polymerase chain reaction analysis. Cell viability was determined using an MTT assay, and the lactate dehydrogenase assay (LDH) was used to investigate cell injury. The expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, Beclin-1, autophagy-related 5 ( Atg5 ), cleaved caspase-3 and cleaved caspase-9 were detected using western blotting. Immunofluorescence assays were performed to detect the expression of LC3 as a marker of autophagy. The target gene of miR-103a-3p was identified using dual-luciferase reporter assays. The results revealed that the expression levels of miR-103a-3p were significantly downregulated in cardiomyocytes under H/R conditions. Injury of the cardiomyocytes was evaluated under H/R conditions. Following transfection of the cells with miR-103a-3p inhibitors, cell injury was increased, as determined by LDH and MTT assays. The expression levels of apoptotic proteins were consistent with the results obtained in the LDH and cell viability assays. The induction of autophagy was increased in cells under H/R conditions and cells with miR-103a-3p inhibitor transfection, whereas the induction of autophagy was decreased in cells transfected with miR-103a-3p mimics. In addition, the data indicated that miR-103a-3p directly targeted Atg5 , which regulated the induction of autophagy and apoptosis. Taken together, these findings indicate that, following the inhibition of miR-103a-3p, Atg5 promotes autophagy and apoptosis in cardiomyocytes by directly targeting Atg5 . Therefore, miR-103a-3p can be considered a potential therapeutic target for myocardial ischemia.

show abstract

“…Moreover, the present study indicated that apoptosis and autophagy exerted negative effects on H9c2 cells during H/r injury. a number of mirs, such as mir-1, mir-195 and mir-320, could regulate numerous signaling molecules to reduce the risk of myocardial apoptosis and autophagy (39)(40)(41). in the present study, significantly decreased expression levels of mir-494 were detected in H/r-treated H9c2 cells compared with control cells, which was similar to a previous study that reported that mir-494 was associated with i/r-induced cardiac injury (20).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑494 suppresses hypoxia/reoxygenation‑induced cardiomyocyte apoptosis and autophagy via the PI3K/AKT/mTOR signaling pathway by targeting SIRT1

Ning

et al. 2020

Mol Med Rep

View full text Add to dashboard Cite

acute myocardial infarction can be caused by ischemia/reperfusion (i/r) injury; however, the mechanism underlying i/r is not completely understood. The present study investigated the functions and mechanisms underlying microrna (mir)-494 in i/r-induced cardiomyocyte apoptosis and autophagy. Hypoxia/reoxygenation (H/r)-treated H9c2 rat myocardial cells were used as an in vitro i/r injury model. apoptosis and autophagy were analyzed by cell counting Kit-8 assay, lactic dehydrogenase and superoxide dismutase assay, flow cytometry, TUNEL staining and western blotting. reverse transcription-quantitative Pcr demonstrated that, H9c2 cells treated with 12 h hypoxia and 3 h reoxygenation displayed significantly downregulated mir-494 expression levels compared with control cells. compared with the corresponding negative control (nc) groups, mir-494 mimic reduced H/r-induced cell apoptosis and autophagy, whereas mir-494 inhibitor displayed the opposite effects. Silent information regulator 1 (SIRT1) was identified as a target gene of mir-494. Furthermore, mir-494 inhibitor-mediated effects on H/r-induced cardiomyocyte apoptosis and autophagy were partially reversed by SirT1 knockdown. Moreover, compared with si-nc, SirT1 knockdown significantly increased the phosphorylation levels of Pi3K, aKT and mTor in H/r-treated and mir-494 inhibitor-transfected H9c2 cells. collectively, the results indicated that mir-494 served a protective role against H/r-induced cardiomyocyte apoptosis and autophagy by directly targeting SirT1, suggesting that mir-494 may serve as a novel therapeutic target for myocardial i/r injury.

show abstract

MiR-320 regulates cardiomyocyte apoptosis induced by ischemia–reperfusion injury by targeting AKIP1

Cited by 45 publications

References 37 publications

Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Circulating miR-320a as a Predictive Biomarker for Left Ventricular Remodelling in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

Effects of miR‑103a‑3p on the autophagy and apoptosis of cardiomyocytes by regulating Atg5

MicroRNA‑494 suppresses hypoxia/reoxygenation‑induced cardiomyocyte apoptosis and autophagy via the PI3K/AKT/mTOR signaling pathway by targeting SIRT1

Contact Info

Product

Resources

About