MicroRNAs regulate mitochondrial apoptotic pathway in myocardial ischemia-reperfusion-injury

Makhdoumi, Pouran; Roohbakhsh, Ali; Karimi, Gholamreza

doi:10.1016/j.biopha.2016.10.073

Cited by 65 publications

(43 citation statements)

References 136 publications

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“…We both demonstrated the down-regulated effect of H 2 S on apoptosis induced by I/R as well as the cardio-protection. In the present study, the biomarkers of apoptosis, including Caspase-3, Caspase-8, Caspase-9, were all down-regulated by H 2 S. Apoptosis is a complicated and accuratelymediated process involving numerous molecules and pathways [23]. Studies have found the PI3K/Akt pathway is associated with cardiomyocytes apoptosis induced by I/R [36,37].…”

Section: Bioinformatic Analysis and Luciferase Assay In The Present Ssupporting

confidence: 48%

“…MIRI is now considered a major cause leading to the worse prognosis of AMI patients, despite early revascularization therapies [22]. Numerous studies focusing on MIRI demonstrated that the endogenous ROS caused by I/R and apoptosis could play a vital role in the process of cardiac injury [23,24]. In the present study, we used the rats and H9c2 cells to build the I/R model and found that transfection with lncRNA Oprm1 could mitigate MIRI and reduces apoptosis.…”

Section: Discussionmentioning

confidence: 71%

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Overexpression of Long noncoding RNA Oprm1 Attenuates Myocardial Ischemia/Reperfusion Injury by Increasing Endogenous Hydrogen Sulfide Production via Oprm1/miR-30b-5p/CSE axis

Hu¹,

Liu²,

Wu³

et al. 2020

Preprint

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Background: Ischemia/Reperfusion (I/R) Injury largely limits the efficacy of revascularization in acute myocardial infarction. Long noncoding RNA (lncRNA) Oprm1 is protective in cerebral I/R injury. However, the effect of lncRNA Oprm1 on myocardial I/R injury and its mechanism remains unknown.Methods: We ligated and then released the left anterior descending coronary artery of adult male rats to build the I/R model in vivo, while an H9c2 cardiomyocytes hypoxia-reoxygenation (H/R) model was also used. Myocardial infarction area, cardiac function, histology, Tunnel staining, cell viability, and vital protein expression was conducted and compared.Results: lncRNA Oprm1 was significantly down-regulated in the I/R injury model. When administered with the AAV9-Oprm1 vector, the myocardial injury and cardiac function were mitigated and preserved, with apoptosis reduced. The cystathionine-γ-lyase (CSE) expression and hydrogen sulfide (H2S) expression were increased. The dual-luciferase reporter gene revealed the targeted relationship between lncRNA Oprm1 and miR-30b-5p. In H9c2 cardiomyocytes models, the miR-30b-5p blocked the protective effect of lncRNA Oprm1 on H/R injury, when Bcl-2, Bcl-xl was down-regulated, and HIF-1α, Bnip-3, Caspase-3, and Caspase-9 up-regulated.Conclusions: lncRNA Oprm1can competitively combines with miR-30b-5p, which down-regulates the expression of CSE. When administered with lncRNA Oprm1, increased endogenous H2S can reduce apoptosis and protect the myocardium from I/R injury via activating PI3K/Akt pathway and inhibiting HIF1-α activity.

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Section: Bioinformatic Analysis and Luciferase Assay In The Present Ssupporting

confidence: 48%

Section: Discussionmentioning

confidence: 71%

Overexpression of Long noncoding RNA Oprm1 Attenuates Myocardial Ischemia/Reperfusion Injury by Increasing Endogenous Hydrogen Sulfide Production via Oprm1/miR-30b-5p/CSE axis

Hu¹,

Liu²,

Wu³

et al. 2020

Preprint

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“…Studies have increasingly revealed the potential roles of miRNAs as diagnostic biomarkers or therapeutic targets in the treatment of myocardial I/R (11,14). For example, miR-29a and let7 elicited cardioprotective effects by regulating insulin-like growth factor-1, which inhibits the cell apoptotic signaling pathway following myocardial I/R, thereby offering theoretical (26,27). Several studies have focused on methods of alleviating the cell death of myocardiocytes to attenuate myocardial I/R injury.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑221‑3p contributes to cardiomyocyte injury in H2O2‑treated H9c2 cells and a rat model of myocardial ischemia‑reperfusion by targeting p57

et al. 2018

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Myocardial ischemia‑reperfusion (I/R) injury is a major cause of cardiovascular disease worldwide, and microRNAs have been implicated in the regulation of pathological and physiological processes in myocardial I/R injury. The present study aimed to investigate the role of microRNA (miR)‑221‑3p in myocardial I/R injury. Cell death and lactate dehydrogenase (LDH) activity were increased in hydrogen peroxide (H2O2)‑treated H9c2 cells, as measured by flow cytometry and an LDH detection kit. The expression of miR‑221‑3p was elevated in H2O2‑incubated cells and in remote areas of the rat I/R model, examined using reverse transcription‑quantitative polymerase chain reaction analysis. The overexpression of miR‑221‑3p enhanced the number of propidium iodide (PI)+ cells and the activity of LDH in H2O2‑treated cells. In I/R‑induced rats, the overexpression of miR‑221‑3p promoted the number of myosin+ cells and inhibited the fractional shortening of left ventricular diameter (FSLVD%). The results showed that the expression of p57 at the gene and protein levels was decreased in H9c2 cells incubated with H2O2 and in rats subjected to I/R surgery; the expression of p57 decreased following the overexpression of miR‑221‑3p. Subsequently, the hypothesis that p57 was the direct target of miR‑221‑3p was confirmed by performing a dual‑luciferase reporter assay. Finally, to examine the function of p57 in myocardial impairment, p57 was transfected into H9c2 cells and administered to the rats prior to undergoing H2O2 treatment and I/R surgery, respectively. The results indicated that p57 attenuated the number of PI+ cells and the activity of LDH in H2O2‑treated cells, whereas p57 downregulated the number of myosin+ cells and upregulated FSLVD% in the I/R‑treated rats. Therefore, these findings suggested that miR‑221‑3p exacerbated the H2O2‑induced myocardial damage in H9c2 cells and myocardial I/R injury in the rat model by modulating p57.

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“…Overexpressed lncRNA HOTAIRM1 contributes to glioblastoma tumor growth and invasion [8]. MiRNAs are also identified as a regulator in a wide range of biological processes and are reported to interact with lncRNA, forming a regulatory network at post-transcriptional level [9,10]. LncRNA nuclear paraspeckle assembly transcript TTC TCT AGT GTT CCT CAT GGC TCC TGC AAT GCT AGG ACT C STAT3 CGC ACT TTA GAT TCA TTG ATG C AGG TGA GGG ACT CAA ACT G TULP3 AGC CAA CTA CCT TAT CTC CA AGG TTG GAT CTA AGC TTG C miR-770-5p GUA CCA CGU GUC AGG GC CTC TAC AGC TAT ATT GCC AGC CAC miR-4739 GGG AGG AGA GGC GGA G CTC TAC AGC TAT ATT GCC AGC CAC miR-4688 GGC AGC AGA GGA CCU GG CTC TAC AGC TAT ATT GCC AGC CAC GAPDH GAA GGT GAA GGT CGG AGT C GAA GAT GGT GAT GGG ATT TC U6 ATT GGA ACG ATA CAG AGA AGA TT GGA ACG CTT CAC GAA TTT G 1 (NEAT1) was reported as an oncogene in breast cancer [11], osteosarcoma [12] and hepatocellular carcinoma [13].…”

Section: Introductionmentioning

confidence: 99%

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

et al. 2020

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Long noncoding RNAs (lncRNAs) were viewed as crucial participants in the pathogenesis of abdominal aortic aneurysm (AAA). LncRNA NEAT1 was recognized as an oncogenic gene in various diseases. However, its function and mechanism in AAA were not precisely documented. Here, we explored the functional role and molecular mechanism of NEAT1 in AAA. Functionally, the effect of NEAT1 on the proliferation was assessed by CCK-8 and EdU assay, while its impact on the apoptosis was evaluated through caspase-3/9 activity and TUNEL assays. As a result, we found that NEAT1 knockdown enhanced the proliferation and impaired the apoptosis of vascular smooth muscle cells (VSMCs). Reversely, overexpressed NEAT1 exerted anti-proliferation and pro-apoptosis effects in VSMCs. Mechanically, we found that STAT3 acted as a transcription factor and contributed to NEAT1 transcription by ChIP and luciferase reporter assays. In addition, NEAT1 was confirmed as a sponge of miR-4688 and thereby increase the expression of TULP3 in VSMCs via RIP assay and RNA pull-down assay. Rescue experiments indicted that TULP3 overexpressing countervailed the impact of NEAT1 depletion on AAA biological processes. Conclusively, lncRNA NEAT1 induced by STAT3 was identified as a ceRNA and facilitated AAA formation by targeting miR-4688/TULP3 axis.

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MicroRNAs regulate mitochondrial apoptotic pathway in myocardial ischemia-reperfusion-injury

Cited by 65 publications

References 136 publications

Overexpression of Long noncoding RNA Oprm1 Attenuates Myocardial Ischemia/Reperfusion Injury by Increasing Endogenous Hydrogen Sulfide Production via Oprm1/miR-30b-5p/CSE axis

Overexpression of Long noncoding RNA Oprm1 Attenuates Myocardial Ischemia/Reperfusion Injury by Increasing Endogenous Hydrogen Sulfide Production via Oprm1/miR-30b-5p/CSE axis

MicroRNA‑221‑3p contributes to cardiomyocyte injury in H2O2‑treated H9c2 cells and a rat model of myocardial ischemia‑reperfusion by targeting p57

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

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