MicroRNA-128-3p aggravates doxorubicin-induced liver injury by promoting oxidative stress via targeting Sirtuin-1

Zhao, Xin; Jin, Yue; Li, Lei; Xu, Lina; Tang, Zeyao; Qi, Yan; Yin, Lianhong; Peng, Jinyong

doi:10.1016/j.phrs.2019.104276

Cited by 81 publications

(63 citation statements)

References 58 publications

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“…Zhao el al. showed that miRNA-128-3p aggravated the doxorubicin-induced liver injury by promoting oxidative stress via targeting SIRT1 [78]. The study of Zhu et al demonstrates a pro-apoptotic role of miRNA-195 in cardiomyocytes and identifies SIRT1 as a direct target of miRNA-195.…”

Section: Sirt1 Pathwaymentioning

confidence: 99%

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

137

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Reactive oxygen species (ROS) are important molecules in the living organisms as a part of many signaling pathways. However, if overproduced, they also play a significant role in the development of cardiovascular diseases, such as arrhythmia, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction and heart transplantation), and heart failure. As a result of oxidative stress action, apoptosis, hypertrophy, and fibrosis may occur. MicroRNAs (miRNAs) represent important endogenous nucleotides that regulate many biological processes, including those involved in heart damage caused by oxidative stress. Oxidative stress can alter the expression level of many miRNAs. These changes in miRNA expression occur mainly via modulation of nuclear factor erythroid 2-related factor 2 (Nrf2), sirtuins, calcineurin/nuclear factor of activated T cell (NFAT), or nuclear factor kappa B (NF-κB) pathways. Up until now, several circulating miRNAs have been reported to be potential biomarkers of ROS-related cardiac diseases, including myocardial infarction, hypertrophy, ischemia/reperfusion, and heart failure, such as miRNA-499, miRNA-199, miRNA-21, miRNA-144, miRNA-208a, miRNA-34a, etc. On the other hand, a lot of studies are aimed at using miRNAs for therapeutic purposes. This review points to the need for studying the role of redox-sensitive miRNAs, to identify more effective biomarkers and develop better therapeutic targets for oxidative-stress-related heart diseases.

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Section: Sirt1 Pathwaymentioning

confidence: 99%

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

137

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“…reported that miRNA-128-3p could aggravate liver injury by promoting oxidative stress via targeting sirtuin-1. 29 Moreover, Wu et al. also found that miR-128-3p was contained in the inflammatory responses of BMSCs, 14 while Surmiak et al.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of microRNA-128-3p alleviates liver ischaemia–reperfusion injury in mice through repressing the Rnd3/NF‐κB axis

et al. 2020

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Although liver ischaemia–reperfusion (I/R) injury remains the primary underlying reason for liver transplant failure or post-transplantation liver dysfunction, the underlying mechanism is still largely elusive. MicroRNAs (miRNA) are involved in multiple physiological and pathological processes, including inflammation. Here, we identified that the miR-128-3p/Rho family GTPase 3 (Rnd3)/NF‐κB axis might play a critical role in liver I/R injury. Our results demonstrated that the level of miR-128-3p was negatively correlated with the Rnd3 level during liver I/R. Dual luciferase reporter assay results proved that Rnd3 mRNA was a direct target of miR-128-3p. Additionally, Western blotting and quantitative RT-PCR analyses revealed that knock-down of miR-128-3p could up-regulate Rnd3 mRNA and protein levels, thereby suppressing the NF-κB pathway through down-regulating NF‐κB p65. Consequently, the serum levels of NF-κB–associated inflammatory factors and aspartate aminotransferase/alanine aminotransferase were decreased. Moreover, overexpression of Rnd3 could reverse the activation of NF-κB caused by miR-128-3p agomir during liver I/R injury. Overall, our study results suggest that repression of miR-128-3p can alleviate liver I/R injury through the miR-128-3p/Rnd3/NF‐κB axis and may facilitate the development of novel protective approaches against liver I/R injury.

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“…miR-212-3p inhibits LPSinduced inflammatory responses by targeting high mobility group box − 1 in mouse macrophages [11]. miR-128-3p plays an important role in Dox-induced liver injury by targeting Sirt1 [12]. However, whether miR-128-3p participates in the anti-inflammatory activity of dexmedetomidine in ALI remains unclear.…”

Section: Introductionmentioning

confidence: 99%

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

Ding¹,

Gao²,

Yu³

et al. 2020

J Bioenerg Biomembr

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Background: To investigate the role of miR-128-3p and MAPK14 in the dexmedetomidine treatment of acute lung injury in septic mice. Methods: SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO 2 , PaCO 2 , MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to detect the targeting relationship of miR-128-3p and MAPK14, and qPCR and WB were used to detect the expression of miR-128-3p and MAPK14. Results: Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased (all p < 0.05). Compared with the Model group, the contents of MDA, MPO, inflammatory factors in the DEX group and miR-128-3p mimic group were significantly decreased, and the content SOD was significantly increased, however, opposite results were occurred in oe-MAPK14 group (all p < 0.05). Compared with the DEX group, all the indicators in miR-128-3p mimic+DEX group showed significant improvement (all p < 0.05). Compared with the miR-128-3p mimic group, all the indicators were deteriorated in the miR-128-3p mimic+oe-MAPK14 group (all p < 0.05). The combination of DEX and oe-MAPK14 blocked the protective effect of dexmedetomidine on acute lung injury in septic mice. Conclusion: miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

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MicroRNA-128-3p aggravates doxorubicin-induced liver injury by promoting oxidative stress via targeting Sirtuin-1

Cited by 81 publications

References 58 publications

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Inhibition of microRNA-128-3p alleviates liver ischaemia–reperfusion injury in mice through repressing the Rnd3/NF‐κB axis

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

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