miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11

Yang, Tianshu; Cao, Changyu; Yang, Jie; Liu, Tianqi; Lei, Xin Gen; Zhang, Ziwei; Xu, Shiwen

doi:10.1016/j.redox.2017.11.025

Cited by 127 publications

(73 citation statements)

References 50 publications

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“…As shown in Figure A,B, compared to the control group, mitochondrial membrane potential was reduced to near‐normal levels. Interestingly, resveratrol treatment reversed mitochondrial membrane potential, as evidenced by increased red‐to‐green fluorescence ratio . Besides, mitochondrial function was also determined via measuring adenosine triphosphate (ATP) content in N2a cells.…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, resveratrol treatment reversed mitochondrial membrane potential, as evidenced by increased red-to-green fluorescence ratio. 59,60 Besides, mitochondrial function was also determined via measuring adenosine triphosphate (ATP) content in N2a cells. As shown in Figure 3C, compared to the control group, HR injury reduced ATP production in N2a cells, and this alteration could be reversed by high dose resveratrol.…”

Section: Resveratrol Modulates Mitochondrial Function and Energy Mementioning

confidence: 99%

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Resveratrol attenuates cerebral ischaemia reperfusion injury via modulating mitochondrial dynamics homeostasis and activating AMPK‐Mfn1 pathway

Gao

Wang

et al. 2019

Int J Experimental Path

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Summary The pathogenesis of cerebral ischaemia reperfusion injury (IRI) has not been fully described. Accordingly, there is little effective drug available for the treatment of cerebral IRI. The aim of our study was to explore the exact role played by Mfn1‐mediated mitochondrial protection in cerebral IRI and evaluate the beneficial action of resveratrol on reperfused brain. Our study demonstrated that hypoxia‐reoxygenation (HR) injury caused N2a cell apoptosis and this process was highly affected by mitochondrial dysfunction. Decreased mitochondrial membrane potential, increased mitochondrial oxidative stress, and an activated mitochondrial apoptosis pathway were noted in HR‐treated N2a cells. Interestingly, resveratrol treatment could attenuate N2a cell apoptosis via sustaining mitochondrial homeostasis. Further, we found that resveratrol modulated mitochondrial performance via activating the Mfn1‐related mitochondrial protective system. Knockdown of Mfn1 could abolish the beneficial effects of resveratrol on HR‐treated N2a cells. Besides, we also report that resveratrol regulated Mfn1 expression via the AMPK pathway; inhibition of AMPK pathway also neutralized the anti‐apoptotic effect of resveratrol on N2a cells in the setting of cerebral IRI. Taken together our results show that mitochondrial damage is closely associated with the progression of cerebral IRI. In addition we also demonstrate the protective action played by resveratrol on reperfused brain and show that this effect is achieved via activating the AMPK‐Mfn1 pathway.

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Section: Resultsmentioning

confidence: 99%

Section: Resveratrol Modulates Mitochondrial Function and Energy Mementioning

confidence: 99%

Resveratrol attenuates cerebral ischaemia reperfusion injury via modulating mitochondrial dynamics homeostasis and activating AMPK‐Mfn1 pathway

Gao

Wang

et al. 2019

Int J Experimental Path

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“…Previous studies also indicate that miRNAs confer function through specific targeting of molecules correlated with necroptosis. For example, miR-200a-5p binds with ring finger protein 11 to trigger RIPK3dependent necroptosis in vivo and in vitro (22). However, it is unknown whether miRNAs modulate renal injury by directly targeting the central mediator of the necroptotic pathway, specifically MLKL.…”

Section: Discussionmentioning

confidence: 99%

hsa‐miR‐500a‐3P alleviates kidney injury by targeting MLKL‐mediated necroptosis in renal epithelial cells

Jiang

Liu

et al. 2018

FASEB j.

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MLKL is a central mediator for necroptosis. Its knockout significantly relieves acute kidney injury (AKI). However, its upstream regulatory mechanism in AKI has not been fully elucidated. We recently reviewed how microRNAs (miRNAs), a type of well‐studied epigenetic regulator, play critical roles in AKI. Here, we evaluated miRNAs that potentially target MLKL and evaluated their function in human tubular epithelial cells in response to toxic and ischemic insults. TargetScan analysis showed that miR‐194‐5P, miR‐338‐3P, miR‐500a‐3P, and miR‐577 had MLKL binding sites. Although all 4 miRNAs are reduced in AKI, our data show that only hsa‐miR‐500a‐3P was significantly suppressed in cisplatin‐treated human tubular epithelial (HK2) cells. We further found that hsa‐miR‐500a‐3P alleviated cisplatin‐induced HK2 cell death, which was confirmed by transmission electron microscopy and flow cytometry. In addition, overexpression of hsa‐miR‐500a‐3P decreased kidney injury molecule‐1 mRNA and protein levels. Real‐time PCR, ELISA, and immunofluorescence data show that hsa‐miR‐500a‐3P protected against inflammatory response, evidenced by decreased monocyte chemotactic protein‐1 and proinflammatory cytokines TNF‐α and IL‐8. Further, hsa‐miR‐500a‐3P attenuated P65 NF‐κB phosphorylation and promoter activity. Mechanistically, luciferase reporter assay showed that hsa‐miR‐500a‐3P bound the 3′UTR of MLKL, thereby suppressing phosphorylation and membrane translocation of MLKL. In agreement with these findings, we identified that overexpression of hsa‐miR‐500a‐3P attenuated cell injury and the inflammatory response in response to sodium azide treatment in an in vitro model. Results show that circulating exosomes from patients with AKI down‐regulated miR‐500a‐3P, which suppressed cell injury and inflammation in HK2 cells. hsa‐miR‐500a‐3P alleviated toxic and ischemic insults that were triggered by cell necroptosis and the inflammatory response in human HK2 cells by targeting MLKL. This may serve as a novel therapeutic target for treatment of AKI.—Jiang, L., Liu, X.‐Q., Ma, Q., Yang, Q., Gao, L., Li, H.‐D., Wang, J.‐N., Wei, B., Wen, J., Li, J., Wu, Y.‐G., Meng, X.‐M. hsa‐miR‐500a‐3P alleviates kidney injury by targeting MLKL‐mediated necroptosis in renal epithelial cells. FASEB J. 33, 3523–3535 (2019). http://www.fasebj.org

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“…According to Verjans, heart failure-associated down regulation of the miRNA-221/222 family enables fibrosis signaling in a pressure-overloaded heart in rats [12]. In our previous study, we showed in chickens that regulation of miR-200a-5p and its target gene blocks necroptosis in the heart, which revealed a novel myocardial necrosis regulation model in heart disease [13].…”

Section: Introductionmentioning

confidence: 94%

miR-2954 Inhibits PI3K Signaling and Induces Autophagy and Apoptosis in Myocardium Selenium Deficiency

Liu

Cai

Gao

et al. 2018

Cell Physiol Biochem

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Background/Aims: Selenium (Se) deficiency can lead to several cardiac diseases, including Keshan disease in humans, mulberry heart disease in pigs and cardiac injury in chickens. MicroRNAs have been a research focus in recent years and have been shown to participate in a new avenue of cell death-autophagy, which can play a significant role in several types of heart disease. Methods: MicroRNAome analysis showed that the expression of miR-2954 was increased in the myocardium of selenium-deficient chickens, and PI3K was predicted to be the target gene. The target relationship between miR-2954 and PI3K was verified with a double fluorescence enzyme assay and RNA Protein Interaction Prediction and molecular docking software. qRT-PCR and western blotting were used to detect the expression of PI3K and related pathway components in selenium-deficient chickens and miR-2954 knockout/overexpression cardiomyocytes. Results: In this study, we observed that miR-2954 overexpression led to inhibition of PI3K pathway in vivo and in vitroled to inhibition of the PI3K pathway in vivo and in vitro. Conclusion: The expression of miR-2954 was increased in selenium-deficient myocardium, whereas overexpression of miR-2954 led to autophagy and apoptosis of myocardial cells during cardiac injury through regulation of the PI3K pathway; whether this phenomenon is a self-protection mechanism of the organism or damage caused by miR-2954 requires further study. Our findings provides new insight apoptosis in cardiomyocytes; additionally, we aim to provide a new direction for the diagnosis and targeted treatment of myocardial diseases.

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miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11

Cited by 127 publications

References 50 publications

Resveratrol attenuates cerebral ischaemia reperfusion injury via modulating mitochondrial dynamics homeostasis and activating AMPK‐Mfn1 pathway

Resveratrol attenuates cerebral ischaemia reperfusion injury via modulating mitochondrial dynamics homeostasis and activating AMPK‐Mfn1 pathway

hsa‐miR‐500a‐3P alleviates kidney injury by targeting MLKL‐mediated necroptosis in renal epithelial cells

miR-2954 Inhibits PI3K Signaling and Induces Autophagy and Apoptosis in Myocardium Selenium Deficiency

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