MicroRNA-210 Modulates the Cellular Energy Metabolism Shift During H2O2-Induced Oxidative Stress by Repressing ISCU in H9c2 Cardiomyocytes

Sun, Weiyi; Zhao, Lei; Song, Xianjing; Zhang, Jichang; Xing, Yue; Liu, Ning; Yan, Youyou; Li, Zhibo; Yang, Lu; Wu, Junduo; Li, Longbo; Yang, Xiao; Tian, Xin; Li, Tianyi; Guan, Yinuo; Wang, Yiran; Liu, Bin

doi:10.1159/000480417

Cited by 38 publications

(29 citation statements)

References 47 publications

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“…It should be noted that the controversial effects of miR-210 on cardiomyocytes under hypoxia conditions have been reported. Sun et al and our previous study demonstrated that miR-210 induced oxidative stress, inhibited mitochondrial function, and promoted cell death in fetal cardiomyocytes [89,90]. However, Mutharasan et al showed that overexpression of miR-210 reduced fetal cardiomyocyte death in response to oxidative stress and reduced ROS production through Akt-and p53-dependent pathways [91].…”

Section: Ischemic Heart Diseasementioning

confidence: 83%

Mitochondrial MiRNA in Cardiovascular Function and Disease

Song

Zhang

2019

Cells

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MicroRNAs (miRNAs) are small noncoding RNAs functioning as crucial post-transcriptional regulators of gene expression involved in cardiovascular development and health. Recently, mitochondrial miRNAs (mitomiRs) have been shown to modulate the translational activity of the mitochondrial genome and regulating mitochondrial protein expression and function. Although mitochondria have been verified to be essential for the development and as a therapeutic target for cardiovascular diseases, we are just beginning to understand the roles of mitomiRs in the regulation of crucial biological processes, including energy metabolism, oxidative stress, inflammation, and apoptosis. In this review, we summarize recent findings regarding how mitomiRs impact on mitochondrial gene expression and mitochondrial function, which may help us better understand the contribution of mitomiRs to both the regulation of cardiovascular function under physiological conditions and the pathogenesis of cardiovascular diseases.

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Section: Ischemic Heart Diseasementioning

confidence: 83%

Mitochondrial MiRNA in Cardiovascular Function and Disease

Song

Zhang

2019

Cells

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“…Similarly, in mouse liver, a subset of miRNAs (20 miRNAs) selectively enriched in mitochondria were identified [70]. Apart from the regulation of mitochondrial genome, other studies have also provided evidences that miRNAs were involved in regulating many events related to mitochondrial function like mitochondria-mediated apoptosis [71], OXPHOS and antioxidant enzymes [65], ROS activity and ATP generation [64], mitophagy [72], mitochondrial fission [73], energy metabolism [74], and fatty acid metabolism [64]. A schematic miRNAs biogenesis and translocation into the mitochondria to regulate mt-DNA expression is presented in Figure 2.…”

Section: Crosstalk Between Mitochondria and Micrornas And Its Signifimentioning

confidence: 99%

WITHDRAWN: Mitochondria: a critical target in the toxicity of trichothecenes and potential treatment strategies

Huang¹,

Cui²,

Wu³

et al. 2018

Oncotarget

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Copyright: Huang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACTTrichothecenes are secondary metabolites produced by fungi of genus Fusarium. It was known that trichothecenes can bind to the 60S subunit of the eukaryotic ribosomes, resulting in inhibition of protein synthesis. However, emerging evidences suggest that trichothecenes can target the mitochondria to induce mitochondrial dysfunction and mitochondria-dependent apoptosis. Numerous studies have investigated the mitochondria-associated toxicities induced by trichothecenes. Here, we mainly collected the data associated with mitochondria and its relationship with trichothecene-induced toxic effects. We showed that mitochondria are the main site of reactive oxygen species production and mediate the trichothecene-induced apoptosis in various cells. The mitochondrial membrane permeabilization plays critical roles in this apoptotic process. Trichothecenes can penetrate the mitochondrial membrane due to its amphiphilic property, and inhibit the activities of mitochondrial respiratory chain complexes and electron transfer in mitochondria. Besides, trichothecenes reduce the mitochondrial biogenesis and mitochondrial transcription and translation. Peroxisome proliferator-activated receptor-γ co-activator 1α and mammalian target of rapamycin pathway are closely linked to this process. Trichothecenes can activate various microRNAs that may mediate the protein synthesis inhibition. These microRNAs may have a crosstalk with mitochondria to mediate the mitochondrial dysfunction and transcription repression in mitochondrial genome. Numerous natural compounds have been tested for their effective antioxidant and anti-inflammatorycapacities. Specially, mitochondria-targeted antioxidants and mitophagy exhibit outstanding cytoprotective abilitysince they can reduce the mitochondrial reactive oxygen species and maintain the mitochondrial quality. This review may shed some new light on the mitochondriaassociated mechanism underlying the toxicity of trichothecenes and new preventive ways to combat these mycotoxins. www.impactjournals.com/oncotarget/

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“…Aberrant miRNA expression is associated with the occurrence of cancer in humans, such as colorectal cancer [8] and NSCLC [9]. Recently, miRNA (miR)-210, which is located on chromosome 11p15.5, was found to have multiple roles in various biological processes, such as angiogenesis and regulation of the immune system, by modulating cell proliferation, differentiation, degradation, and necrosis [10], and miR-210 was involved in the myocardial energy metabolism regulating the energy shift in cardiomyocytes during oxidative stress [11]. Deregulation of miR-210 may aberrantly activate oncogenes, deactivate tumor suppressor genes, inhibit DNA repair, and promote angiogenesis, ultimately accelerating the process of carcinogenesis, especially in a hypoxic environment [12].…”

Section: Introductionmentioning

confidence: 99%

Clinical Significance of miR-210 and its Prospective Signaling Pathways in Non-Small Cell Lung Cancer: Evidence from Gene Expression Omnibus and the Cancer Genome Atlas Data Mining with 2763 Samples and Validation via Real-Time Quantitative PCR

Cen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Since the function of microRNA (miR)-210 in non-small cell lung cancer (NSCLC) remains unclear, we aimed to explore the clinical significance of miR-210 in NSCLC. Methods: NSCLC-related data from 1673 samples on Gene Expression Omnibus and 1090 samples on The Cancer Genome Atlas were obtained and analyzed. The expression level of miR-210 was validated via real-time quantitative PCR analysis with 125 paired clinical samples. A meta-analysis was performed to generate a comprehensive understanding of miR-210 expression and its clinical significance in NSCLC. In addition, bioinformatics analysis was also conducted to reveal the potential underlying mechanism of miR-210 action in NSCLC. Results: miR-210 expression was consistently elevated in NSCLC solid tissue samples. However, its expression was controversial in easily obtained body fluids (i.e., blood, plasma, and serum). Moreover, an overall pooled meta-analysis implied a comparatively higher level of miR-210 expression in NSCLC cancerous tissue than in normal control tissue (P < 0.001). In addition, a meta-analysis of outcome revealed a significant diagnostic capacity of miR-210 in NSCLC by detecting its expression in serum and sputum (area under the summary receiver operating characteristic curve 0.82 and 0.81, respectively). miR-210 overexpression was associated with poor progression-free survival (PFS) in NSCLC and was negatively related to overall survival and disease-free survival. Bioinformatic gene enrichment and annotation analyses showed that the target genes of miR-210 were greatly enriched in cell adhesion and plasma membrane, and three pathways were considered to be the main functional circuits of miR-210: renin secretion, the cGMP-PKG signaling pathway, and cell adhesion molecules. Conclusion: In NSCLC, miR-210 expression was elevated and overexpression indicated poor PFS. Expression level of miR-210 in serum and sputum showed significant diagnostic value for NSCLC.

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MicroRNA-210 Modulates the Cellular Energy Metabolism Shift During H2O2-Induced Oxidative Stress by Repressing ISCU in H9c2 Cardiomyocytes

Cited by 38 publications

References 47 publications

Mitochondrial MiRNA in Cardiovascular Function and Disease

Mitochondrial MiRNA in Cardiovascular Function and Disease

WITHDRAWN: Mitochondria: a critical target in the toxicity of trichothecenes and potential treatment strategies

Clinical Significance of miR-210 and its Prospective Signaling Pathways in Non-Small Cell Lung Cancer: Evidence from Gene Expression Omnibus and the Cancer Genome Atlas Data Mining with 2763 Samples and Validation via Real-Time Quantitative PCR

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