miR-190a-5p regulates cardiomyocytes response to ferroptosis via directly targeting GLS2

Zhou, Xiaodao; Zhuo, Mali; Zhang, Yayun; Shi, Erdong; Ma, Xujie; Li, Hong

doi:10.1016/j.bbrc.2021.05.100

Cited by 28 publications

(30 citation statements)

References 21 publications

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“…In order to further verify the interaction between miR-340-5p and MyD88, the RNA pull-down assay was performed according to the method described in previous studies [ 27 , 28 ]. Briefly, Bio-miR-340-5p or Bio-NC (GenePharma; Shanghai, China) was transfected into HL-1 cells based on the Lipofectamine 2000 kit.…”

Section: Methodsmentioning

confidence: 99%

miR-340-5p Alleviates Oxidative Stress Injury by Targeting MyD88 in Sepsis-Induced Cardiomyopathy

Zhang

Zeng

Cai

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Sepsis-induced cardiomyopathy (SIC) is a sort of severe disease in the intensive care unit. This research focuses on exploring the influence of miR-340-5p on SIC and its specific mechanism. Methods. Mice were administered with lipopolysaccharide (LPS) to construct a SIC animal model. Mice were intramyocardially injected with Adenoassociated Virus- (AAV-) 9 containing the miR-340-5p precursor to make the miR-340-5p overexpression in the myocardium. The expression level of myocardial miR-340-5p was evaluated by qRT-PCR. The cardiac function was measured by echocardiography, the myocardial morphology was observed by hematoxylin-eosin (HE) staining, and the oxidative stress level was detected by 4-hydroxynonenal (4-HNE) immunohistochemical staining and malondialdehyde (MDA) assay in mice. The cells were pretreated with miR-340-5p mimic, mimic-NC, miR-340-5p inhibitor, inhibitor-NC, MyD88 siRNA, or si-NC and then administered with LPS or PBS. The cell viability was measured with the CCK-8 assay. The level of intracellular oxidative stress was evaluated using reactive oxygen species (ROS), MDA, and glutathione (GSH) detection. The MyD88 level was assessed via Western blotting analysis. The interaction of miR-340-5p with the MyD88 mRNA was confirmed via dual-luciferase reporter assay and RNA pull-down assay. Results. The miR-340-5p overexpression partially alleviated the increase of the MyD88 level, impairment of cardiac function, and oxidative stress injury in the SIC animal model. In the SIC cell model, miR-340-5p mimic pretreatment partially relieved oxidative stress injury, while the miR-340-5p inhibitor had the opposite effect. Besides, the miR-340-5p mimic and inhibitor could reduce and further increase the MyD88 level in the SIC cell model, respectively. Dual-luciferase reporter and RNA pull-down experiments confirmed the interaction between the MyD88 mRNA and miR-340-5p. Finally, it was found that MyD88 siRNA pretreatment also partially alleviates the oxidative stress injury in the SIC cell model. Conclusion. In sum, our study demonstrated that miR-340-5p can improve myocardial oxidative stress injury by targeting MyD88 in SIC.

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Section: Methodsmentioning

confidence: 99%

miR-340-5p Alleviates Oxidative Stress Injury by Targeting MyD88 in Sepsis-Induced Cardiomyopathy

Zhang

Zeng

Cai

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…BTB and CNC homology 1(Bach1) is an oxidative stressresponsive transcription factor in ferroptosis, which promotes it by inhibiting the antioxidant system (GSH-GPX4 and FSP1-CoQ10 pathways) (Nishizawa et al, 2022). Li et al showed that miR-194-loaded mesenchymal exosomes can inhibit neurovascular endothelial cell ferroptosis by targeting Bach1, resulting in neuroprotection (Li X. et al, 2021). Prostaglandin peroxidase synthase-2(Ptgs2) is a regulatory gene in ferroptosis lipid oxidation (Macías-Rodríguez et al, 2020).…”

Section: The Role Of Microrna In Cardiomyopathy Via Regulating Ferrop...mentioning

confidence: 99%

“…After myocardial infarction, cardiomyocytes often undergo cell death and pathological remodeling, which easily lead to heart failure ( Duan, 2020 ). Zhou et al have suggested that miR-190a-5p inhibits cardiomyocyte ferroptosis by inhibiting GLS2 and decreases the levels of ROS, MDA, and Fe 2+ in H9c2 cells, thus playing a protective role in myocardial infarction ( Zhou et al, 2021 ). MiR-190a-5p reduces lipid peroxidation by inhibiting GLS2 mRNA, thereby inhibiting ferroptosis and lowering the risk of myocardial infarction.…”

Section: Introductionmentioning

confidence: 99%

The role of microRNAs in ferroptosis

Guo

Zhang²,

Liu³

2022

Front. Mol. Biosci.

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Ferroptosis is a newly discovered type of programmed cell death, which is closely related to the imbalance of iron metabolism and oxidative stress. Ferroptosis has become an important research topic in the fields of cardiomyopathy, tumors, neuronal injury disorders, and ischemia perfusion disorders. As an important part of non-coding RNA, microRNAs regulate various metabolic pathways in the human body at the post-transcriptional level and play a crucial role in the occurrence and development of many diseases. The present review introduces the mechanisms of ferroptosis and describes the relevant pathways by which microRNAs affect cardiomyopathy, tumors, neuronal injury disorders and ischemia perfusion disorders through regulating ferroptosis. In addition, it provides important insights into ferroptosis-related microRNAs, aiming to uncover new methods for treatment of the above diseases, and discusses new ideas for the implementation of possible microRNA-based ferroptosis-targeted therapies in the future.

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“…Overexpression of miR-190a-5p will inhibit GLS2 and decrease the accumulation of ROS, MDA, and Fe. At the same time, inhibiting the expression of miR-190a-5p leads to the upregulation of GLS2, which increases the oxidative stress response and ferroptosis [ 57 ]. Moreover, Sun et al found that miR-135b-3p promotes ferroptosis by targeting GPX4, thereby aggravating myocardial ischemia/reperfusion injury.…”

Section: Regulation Of Noncoding Rna On Ferroptosis In Cvdmentioning

confidence: 99%

The Emerging Role of Noncoding RNA Regulation of the Ferroptosis in Cardiovascular Diseases

Zhang

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Cardiovascular disease (CVD) is a significant public health issue due to its high prevalence and considerable contribution to the global disease burden. Recent studies suggest that genetic factors, including noncoding RNAs, have an important role in the progression of CVD. Noncoding RNA plays a critical role in genetic programming and gene regulation during development. Ferroptosis is a form of iron-dependent regulated cell death (RCD), which is mainly caused by increased lipid hydroperoxide and redox imbalance. Ferroptosis is essentially different from other forms of RCD in morphology and mechanism, such as apoptosis, autophagic cell death, pyroptosis, and necroptosis. Much evidence suggested ferroptosis is involved in the development of various CVDs, especially in cardiac ischemia/reperfusion injury, heart failure, and aortic dissection. Here, we review the latest findings based on noncoding RNA regulation of ferroptosis and its involvement in the pathogenesis of CVD and related treatments, aimed at providing insights into the impact of noncoding RNA regulation of ferroptosis for CVD.

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miR-190a-5p regulates cardiomyocytes response to ferroptosis via directly targeting GLS2

Cited by 28 publications

References 21 publications

miR-340-5p Alleviates Oxidative Stress Injury by Targeting MyD88 in Sepsis-Induced Cardiomyopathy

miR-340-5p Alleviates Oxidative Stress Injury by Targeting MyD88 in Sepsis-Induced Cardiomyopathy

The role of microRNAs in ferroptosis

The Emerging Role of Noncoding RNA Regulation of the Ferroptosis in Cardiovascular Diseases

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