Inhibiting microRNA-144 abates oxidative stress and reduces apoptosis in hearts of streptozotocin-induced diabetic mice

Ming, Yu; Liu, Yu; Zhang, Bili; Shi, Yanling; Cui, Lijie; Zhao, Xianxian

doi:10.1016/j.carpath.2015.06.003

Cited by 77 publications

(66 citation statements)

References 36 publications

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“…It was also confirmed that myricitrin treatment inhibited the increase in ROS content in H9c2 cardiomyocytes. Numerous studies have demonstrated that oxidative stress is directly related to apoptosis in the hearts of diabetic patients or animals [32]. Given that myricitrin ameliorated HG-induced oxidative stress, we hypothesized that it subsequently inhibited apoptosis of cardiac myocytes.…”

Section: Discussionmentioning

confidence: 96%

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

et al. 2016

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Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.

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Section: Discussionmentioning

confidence: 96%

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

et al. 2016

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“…Furthermore, analysis of miR expression levels in the hearts of various rat and mouse diabetic models also indicated the abnormal expression of miRNA. Further studies demonstrated that miRs contribute to numerous important pathophysiological processes of DCM, including cardiomyocyte hypertrophy, myocardial fibrosis, cardiomyocyte apoptosis, mitochondrial dysfunction, myocardial electrical remodeling and epigenetic modification (27)(28)(29)(30)(31)(32). The present review discusses the possible role of miRs in the pathogenesis of DCM regarding the above-mentioned processes.…”

Section: Introductionmentioning

confidence: 88%

Role of microRNAs in the pathogenesis of diabetic cardiomyopathy

Liu

2017

Biomedical Reports

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Abstract. The morbidity of diabetes mellitus has been increasing annually. As a progressive metabolic disorder, chronic complications occur in the late stage of diabetes. In addition, cardiovascular diseases account for the major cause of morbidity and mortality among the diabetic population worldwide. Diabetic cardiomyopathy (DCM) is a type of diabetic heart disease. Patients with DCM show symptoms and signs of heart failure while no specific cause, such as coronary disease, hypertension, alcohol consumption, or other structural heart diseases has been identified. The pathogenesis of DCM is complex and has not been well understood until recently. MicroRNAs (miRs) belong to a novel family of highly conserved, short, non-coding, single-stranded RNA molecules that regulate transcriptional and post-transcriptional gene expression. Furthermore, recent studies have demonstrated an association between miRs and DCM. In the current review, the role of miRs in the pathogenesis of DCM is summarized. It was concluded that miRs contribute to the regulation of cardiomyocyte hypertrophy, myocardial fibrosis, cardiomyocyte apoptosis, mitochondrial dysfunction, myocardial electrical remodeling, epigenetic modification and various other pathophysiological processes of DCM. These studies may provide novel insights into targets for prevention and treatment of the disease.

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“…Increasing evidence indicated that miRNAs are involved in oxidative stress [13]. Lots of miRNAs have been identified to have protective effect or damage effect, which is dependent on the role of their target genes, including miR-424 [14], miR-25 [15], miR-103 [16], miR-144 [17] and miR-122 [18]. These outcomes show a strong basis for the importance of miRNAs in the pathogenesis of CVD.…”

Section: Introductionmentioning

confidence: 92%

Down-Regulation of MicroRNA-137 Improves High Glucose-Induced Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells by Up-Regulation of AMPKα1

Wei³

et al. 2016

Cell Physiol Biochem

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Background/Aims: To investigate the effects of miR-137 on high glucose (HG)-induced vascular injury, and to establish the mechanism underlying these effects. Methods: Human umbilical vein endothelial cells (HUVECs) were transfected with miR-137 inhibitor or mimic, and then treated with normal or high glucose. Cell viability and apoptosis were detected by using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. Reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) were detected by fluorescent probe (DCFH-DA), thiobarbituric acid reaction, and the nitroblue tetrazolium assay, respectively. The mRNA and protein expressions of AMPKα1 were determined by qRT-PCR and Western blotting. Results: Down-regulation of miR-137 dramatically reverted HG-induced decreases in cell viability and SOD levels and increases in apoptosis, ROS and MDA levels. Moreover, bioinformatics analysis predicted that the AMPKα1 was a potential target gene of miR-137. Luciferase reporter assay demonstrated that miR-137 could directly target AMPKα1. AMPKα1 overexpression had the similar effect as miR-137 inhibition. Down-regulation of AMPKα1 in HUVECs transfected with miR-137 inhibitor partially reversed the protective effect of miR-137 inhibition on HG-induced oxidative stress in HUVECs. Conclusion: Down-regulation of miR-137 ameliorates HG-induced injury in HUVECs by overexpression of AMPKα1, leading to increasing cellular reductive reactions and decreasing oxidative stress. These results provide further evidence for protective effect of miR-137 inhibition on HG-induced vascular injury.

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Inhibiting microRNA-144 abates oxidative stress and reduces apoptosis in hearts of streptozotocin-induced diabetic mice

Cited by 77 publications

References 36 publications

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

Role of microRNAs in the pathogenesis of diabetic cardiomyopathy

Down-Regulation of MicroRNA-137 Improves High Glucose-Induced Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells by Up-Regulation of AMPKα1

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