Inhibition of Mir-128-3p by Tongxinluo Protects Human Cardiomyocytes From Ischemia/Reperfusion Injury via Upregulation of P70s6k1/P-P70s6k1

Chen, Guihao; Xu, Chuansheng; Yang, Yuejin; Zhang, Jie; Li, Qing

doi:10.1016/s0735-1097(18)30715-0

Cited by 10 publications

(18 citation statements)

References 85 publications

(107 reference statements)

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“…Dysregulation of muscle cell proliferation, differentiation, and muscle regeneration is an important cause of muscle‐related diseases. Some studies have demonstrated that miR‐128, as a muscle‐related miRNA, could inhibit cardiomyocyte migration, proliferation, and regeneration, and could regulate chicken myocardial inflammation (G. H. Chen et al, 2017; J. Liu et al, 2020; Velleman & Harding, 2017). Furthermore, in cell‐culture studies, miR‐128 played a crucial role in the proliferation and differentiation of skeletal muscle satellite cells (SMSCs).…”

Section: Role Of Mir‐128 In Muscle Regeneration and Muscle‐related DImentioning

confidence: 99%

The emerging role of miR‐128 in musculoskeletal diseases

Shang

Shen

Chen

et al. 2020

Journal Cellular Physiology

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MicroRNA-128 (miR-128) is associated with cell proliferation, differentiation, migration, apoptosis, and survival. Genetic analysis studies have demonstrated that miR-128 participates in bone metabolism, which involves bone marrow-derived mesenchymal stem cells, osteoblasts, osteoclasts, and adipocytes. miR-128 also participates in regeneration of skeletal muscles by targeting myoblast-associated proteins. The deregulation of miR-128 could lead to a series of musculoskeletal diseases. In this review, we discuss recent findings of miR-128 in relation to bone metabolism and muscle regeneration to determine its potential therapeutic effects in musculoskeletal diseases, and to propose directions for future research in this significant field.

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Section: Role Of Mir‐128 In Muscle Regeneration and Muscle‐related DImentioning

confidence: 99%

The emerging role of miR‐128 in musculoskeletal diseases

Shang

Shen

Chen

et al. 2020

Journal Cellular Physiology

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“…miR-128-3p was closely involved into the occurrence of oxidative stress and myocardial inflammation induced by lipopolysaccharide [10]. Moreover, inhibiting miR-128-3p expression suppressed apoptosis of cardiomyocytes in response to ischemia/reperfusion [11]. However, the role of miR-128-3p in DOX-induced cardiotoxicity is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR-128-3p Attenuated Doxorubicin-Triggered Acute Cardiac Injury in Mice by the Regulation of PPAR-γ

Zhang

Yang

2021

PPAR Research

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Background. The clinical usefulness of doxorubicin (DOX), an anthracycline with antitumor activity, is limited by its cardiotoxicity. Oxidative stress and myocardial apoptosis were closely associated with DOX-induced cardiac dysfunction. It has been reported that microRNA-128-3p (miR-128-3p) was involved into the regulation of redox balance. However, the role of miR-128-3p in DOX-related cardiac injury remains not yet understood. The aim of this study was to investigate the biological effect of miR-128-3p in DOX-induced cardiotoxicity. Methods. To induce DOX-related acute cardiac injury, mice were subjected to a single injection of DOX. Inhibition of myocardial miR-128-3p was achieved by an adeno-associated virus (AAV9) system carrying a miR-128-3p sponge. Results. The data in our study indicated that miR-128-3p was upregulated in DOX-treated hearts and cardiomyocytes. Inhibition of miR-128-3p attenuated DOX-related cardiac injury and improved cardiac function in mice. Moreover, miR-128-3p inhibition could suppress myocardial inflammatory response, oxidative damage, and cell apoptotic death in DOX-treated mice. Further analysis showed that miR-128-3p could directly target peroxisome proliferator-activated receptor γ (PPAR-γ) and decrease PPAR-γ expression. Moreover, the protective effects provided by miR-128-3p inhibition were abolished by a PPAR-γ antagonist in vivo and in vitro. Conclusions. miR-128-3p inhibition attenuated DOX-related acute cardiac injury via the regulation of PPAR-γ in mice.

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“…Chen et al declared that the inhibition of miR-128-3p could regulate the phosphorylation of p70s6k1 to protect human cardiomyocytes from I/R injury. 28 reporter assay demonstrated that miR-128-3p could bind straight to Rnd3 mRNA. *P < 0.05; **P < 0.01 vs. miR-128-3p negative control (NC) in WT group; ns P < 0.05 vs. miR-128-3p NC in mutant group; ## P < 0.01. could aggravate liver injury by promoting oxidative stress via targeting sirtuin-1.…”

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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Inhibition of Mir-128-3p by Tongxinluo Protects Human Cardiomyocytes From Ischemia/Reperfusion Injury via Upregulation of P70s6k1/P-P70s6k1

Cited by 10 publications

References 85 publications

The emerging role of miR‐128 in musculoskeletal diseases

The emerging role of miR‐128 in musculoskeletal diseases

Inhibition of miR-128-3p Attenuated Doxorubicin-Triggered Acute Cardiac Injury in Mice by the Regulation of PPAR-γ

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

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