MicroRNA-30c-5p protects against myocardial ischemia/reperfusion injury via regulation of Bach1/Nrf2

Sun, Meng; Guo, Min; Ma, Guijin; Zhang, Nan; Pan, Feifei; Fan, X S; Wang, Rui

doi:10.1016/j.taap.2021.115637

Cited by 25 publications

(17 citation statements)

References 44 publications

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“…CircSCAF11 overexpression inhibited ROS production by acting as a sponge of miR-145-5p in glioma, which is a cause of glioma initiation and metastasis [ 85 ]. MiR-30c-5p was reported to be an important OS regulator by multiple studies [ 86 – 88 ]. In colorectal cancer, circ3823 functioned as a ceRNA of miR-30c-5p, alleviating the repressive effect of miR-30c-5p on TCF7 which upregulated MYC and CCND1 and eventually led to cancer initiation and metastasis [ 89 ].…”

Section: The Mechanisms Of Ros-ncrnas Axis In Cancer Progressionmentioning

confidence: 99%

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

Zuo

Zhang

et al. 2022

Mol Cancer

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Oxidative stress (OS), characterized by the excessive accumulation of reactive oxygen species (ROS), is an emerging hallmark of cancer. Tumorigenesis and development driven by ROS require an aberrant redox homeostasis, that activates onco-signaling and avoids ROS-induced programmed death by orchestrating antioxidant systems. These processes are revealed to closely associate with noncoding RNAs (ncRNAs). On the basis of the available evidence, ncRNAs have been widely identified as multifarious modulators with the involvement of several key redox sensing pathways, such as NF-κB and Nrf2 signaling, therefore potentially becoming effective targets for cancer therapy. Furthermore, the vast majority of ncRNAs with property of easy detected in fluid samples (e.g., blood and urine) facilitate clinicians to monitor redox homeostasis, indicating a novel method for cancer diagnosis. Herein, focusing on carcinoma initiation, metastasis and chemoradiotherapy resistance, we aimed to discuss the ncRNAs-ROS network involved in cancer progression, and the potential clinical application as biomarkers and therapeutic targets.

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Section: The Mechanisms Of Ros-ncrnas Axis In Cancer Progressionmentioning

confidence: 99%

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

Zuo

Zhang

et al. 2022

Mol Cancer

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“…MicroRNA (miRNA) is a type of endogenous non-coding RNA existing in eukaryotes and is approximately 18–25 nt in length. Previous studies have shown that microRNAs ameliorate MI/R injury [ 7–9 ]. Studies have confirmed that miR-21 expression is significantly reduced after MI/R, and that miR-21 overexpression can decrease the myocardial infarction area and cardiomyocyte apoptosis during chronic ischemia reperfusion injury [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Zhang

Shang

et al. 2021

Bioengineered

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The objective of this study was to explore the effect of argon preconditioning on myocardial ischemia reperfusion (MI/R) injury and its mechanism. Cardiomyocytes H2C9 were pre-treated with 50% argon, and a cell model of oxygen-glucose deprivation (OGD) was established. CCK-8 and cytotoxicity detection kits were used to detect cell viability and lactate dehydrogenase (LDH) release. The miR-21 expression was detected using quantitative real-time polymerase chain reaction. Western blot analysis was performed to detect the expression of programmed cell death protein 4 (PDCD4) and homologous phosphatase and tensin homolog (PTEN) proteins. The levels of inflammatory factors (IL-1β, IL-6, and IL-8) and oxidative stress factors (reactive oxygen species ROS], malondialdehyde [MDA], and superoxide dismutase [SOD]) were measured using an enzyme-linked immunosorbent assay. The effect of argon on cell apoptosis was detected using flow cytometry. Argon increased the proliferation of cardiomyocytes induced by OGD, decreased the release of LDH in cell culture medium, increased miR-21 expression in cells, decreased the expression of miR-21 target proteins PDCD4 and PTEN, decreased the levels of inflammatory factors , and interleukin-8 ) and oxidative stress factors (ROS and MDA), increased the SOD content, and decreased the cell apoptosis rate. Our results suggest that argon preconditioning inhibited the PDCD4/PTEN pathway via miR-21, thereby inhibiting ROS oxidative stress and preventing MI/R injury.

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“…for instance, sev is available to modulate insulin-like growth factor 1 expression through mir-214 to stimulate liver injury [ 13 ], and sev can decline neuroinflammation caused by ciri via up-regulating mir-203 with targeting myd88 after treatment [ 14 ]. MiR-30 c-5p is demonstrated as a vital modulator of some myocardial abnormalities and is usually applied as a therapeutic target to alleviate myocardial ischemia-reperfusion injury [ 15–17 ]. Nevertheless, few studies on mir-30 c-5p in ciri are manifested.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane protects against cerebral ischemia/reperfusion injury via microrna-30c-5p modulating homeodomain-interacting protein kinase 1

et al. 2021

Bioengineered

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Sevoflurane (SEV) has been reported to be an effective neuroprotective agent for cerebral ischemia/reperfusion injury (CIRI). However, the precise molecular mechanisms of Sev preconditioning in CIRI remain largely unknown. Therefore, CIRI model was established via middle cerebral artery occlusion method. SEV was applied before modeling. after successful modeling, lentivirus was injected into the lateral ventricle of the brain. Neurological impairment score was performed in each group, and histopathologic condition, infarct volume, apoptosis, inflammation, oxidative stress, microRNA (miR)-30 c-5p and homeodomain-interacting protein kinase 1 (HIPK1) were detected. Mouse hippocampal neuronal cell line HT22 cells were pretreated with SEV, and the in vitro model was stimulated via oxygen-glucose deprivation and reoxygenation. The corresponding plasmids were transfected, and the cell growth was detected, including inflammation and oxidative stress, etc. The targeting of miR-30 c-5p with HIPK1 was examined. The results clarified that reduced miR-30 c-5p and elevated HIPK1 were manifested in CIRI. SEV could improve CIRI and modulate the miR-30 c-5p-HIPK1 axis in vitro and in vivo , and miR-30 c-5p could target HIPK1. Depressed miR-30 c-5p could eliminate the protection of SEV in vitro and in vivo . Repression of HIPK1 reversed the effect of reduced miR-30 c-5p on CIRI. Therefore, it is concluded that SEV is available to depress CIRI via targeting HIPK1 through upregulated miR-30 c-5p.

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MicroRNA-30c-5p protects against myocardial ischemia/reperfusion injury via regulation of Bach1/Nrf2

Cited by 25 publications

References 44 publications

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Sevoflurane protects against cerebral ischemia/reperfusion injury via microrna-30c-5p modulating homeodomain-interacting protein kinase 1

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