MicroRNA-142-3p inhibits hypoxia/reoxygenation-induced apoptosis and fibrosis of cardiomyocytes by targeting high mobility group box 1

Wang, Yi; Ouyang, Ming; Wang, Qiong; Jian, Zaijin

doi:10.3892/ijmm.2016.2756

Cited by 80 publications

(58 citation statements)

References 31 publications

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“…The study indicated that inhibitors of miR-874 could be useful in the treatment of heart failure via decreasing cardiomyocyte necrosis [36]. Recent studies have also reported that miR-30c-3p and miR-142-3p may participate in the development of myocardial fibrosis by regulating the TGF-β1/Smad3 signaling pathway [37, 38]. Thus, of the 11 identified miRNAs, the roles of miR-370, miR-323, miR-136, miR-142-3p, miR-92b-5p, miR-874 and miR-30c-3p in cardiovascular diseases have been clarified in previous studies, but the functions or mechanisms of miR-491, miR-425, miR-493, and miR376a have not been reported.…”

Section: Discussionmentioning

confidence: 99%

MiRNA Expression Profile of the Myocardial Tissue of Pigs with Coronary Microembolization

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: Coronary microembolization (CME) is a serious complication of coronary heart disease and is considered as a strong predictor of poor long-term prognosis and major cardiac adverse events. Here, we identified differentially expressed microRNAs (miRNAs) in the myocardial tissue of CME pigs, and predicted and analyzed the possible functions of their target genes. Methods: Twelve Bama mini-pigs were randomly assigned to the sham and CME group (n = 6 in each group). The two groups were compared with regard to heart function, area of infarction, cardiomyocyte apoptosis, and myocardial expression of TNF-α, IL-1β and IL-6. Further, miRNA chip analysis was used to screen for differentially expressed miRNAs, and the results were validated by real-time PCR. Bioinformatics methods were used to predict and analyze the functions of the target genes of the identified miRNAs. Results: The model CME pigs showed significantly increased expression of TNF-α, IL-1β and IL-6, as well as micro-infarction lesions and cell apoptosis in the myocardial tissue. Thus, the model was established successfully. In the myocardial tissue of the CME pigs, the expression of ssc-miR-92b-5p, ssc-miR-491, ssc-miR-874, ssc-miR-425-3p, ssc-miR-376a-5p, ssc-miR-370, ssc-miR-30c-3p, ssc-miR-493-5p and ssc-miR-323 was significantly increased, whereas the expression of ssc-miR-136 and ssc-miR-142-3p was significantly decreased. GO and KEGG pathway analysis indicated that the target genes of these miRNAs are mainly associated with cell proliferation, apoptosis, necrosis, inflammation, and fibrosis. Conclusion: The differentially expressed miRNAs identified in the myocardial tissue of CME pigs could be new biomarkers or potential treatment targets for CME.

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Section: Discussionmentioning

confidence: 99%

MiRNA Expression Profile of the Myocardial Tissue of Pigs with Coronary Microembolization

Zhao

et al. 2017

Cell Physiol Biochem

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“…A study by Wang et al (32) reported that miR-142-3p suppressed NF-κB, TNF-α and IL-6 in a murine model of osteoarthritis by targeting HMGB1. Additionally, miR-142-3p targets HMGB1 to inhibit hypoxia/reoxygenation-induced cardiomyocyte apoptosis and fibrosis (61). miR-142-3p is also reported to inhibit tumor growth of lung cancer through targeting HMGB1 (62).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-142-3p relieves neuropathic pain by targeting high mobility group box 1

et al. 2017

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MicroRNA (miRNA) are emerging as critical regulators of neuropathic pain development. Neuroinflammation contributes to the development of neuropathic pain. miR‑142‑3p has been characterized as an inflammation‑related miRNA in various pathological processes. However, little is known about the role of miR‑142‑3p in neuroinflammation and neuropathic pain. The present study aimed to investigate the function of miR‑142‑3p in neuropathic pain by creating a murine model using spinal nerve ligation (SNL). A significant reduction in miR‑142‑3p expression was observed in the dorsal root ganglion of mice with SNL (P<0.05) compared with control mice. Overexpression of miR‑142‑3p significantly inhibited neuropathic pain and neuroinflammation in mice with SNL (P<0.05). High mobility group box 1 (HMGB1) was identified as a direct target gene of miR‑142‑3p by bioinformatic analysis and dual‑luciferase reporter assays. Overexpression of miR‑142‑3p significantly reduced the mRNA and protein expression levels of HMGB1 in vitro and in vivo (P<0.05). In addition, HMGB1 mRNA expression and miR‑142‑3p expression were inversely correlated in mice with SNL. Furthermore, overexpression of HMGB1 significantly reversed the inhibitory effect of miR‑142‑3p on neuroinflammation and neuropathic pain development (P<0.05). Overall, these results suggest that miR‑142‑3p functions as a negative regulator of neuropathic pain development through the downregulation of HMGB1, indicating that miR‑142‑3p may serve as a potential therapeutic target for neuropathic pain.

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“…Zhang et al indicated that miR-142-3p inhibits non-small cell lung carcinoma (NSCLC) cell proliferation and induces cell apoptosis via targeting HMGB1 [30]. In addition, it has been shown that miR-142-3p is a key regulator of cardiomyocytes apoptosis and fibrosis induced by hypoxia/ reoxygenation [14], therefore serving as a candidates for myocardial injury therapeutic strategy. A recent study done by Bao et al demonstrated that platelet-derived miR-142-3p is delivered into ECs via platelet-derived microparticles (PMPs) and induces ECs apoptosis in hypertension through modulating the expression of target molecule BCL2L1 [31].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-142-3p inhibits hypoxia/reoxygenation-induced apoptosis and fibrosis of cardiomyocytes, partly at least, by the direct inhibition of HMGB1 expression [14]. Exosomal miR-142-3p is increased during cardiac allograft rejection and compromises endothelial barrier function via down-regulation of RAB11FIP2 [15].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-142-3p Induces Atherosclerosis-Associated Endothelial Cell Apoptosis by Directly Targeting Rictor

Qin

Shu

Long

et al. 2018

Cell Physiol Biochem

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Background/Aims: Atherosclerosis, a multifactorial chronic disease, is the main cause of death and impairment in the world. Endothelial cells (ECs) apoptosis plays a crucial role in the onset and development of atherosclerosis, whereas the underlying molecular mechanisms are unclear. MicroRNA-142-3p (miR-142-3p) is a well-defined tumor suppressor in several types of cancer, while the role of miR-142-3p in ECs apoptosis and the development of atherosclerosis has yet to be elucidated. Therefore, the present study aimed to investigate the role of miR-142-3p in ECs apoptosis during atherosclerosis and the underlying mechanism. Methods: Human aortic endothelial cells (HAECs) were treated with oxidized low-density lipoprotein (ox-LDL). The expression level of miR-142-3p was detected using qRT-PCR. Apoptosis was determined via flow cytometry and Caspase-3 activity assay. Prediction of the binding between miR-142-3p and 3’-UTR of Rictor mRNA was performed by bioinformatics analyses and confirmed by a dual luciferase reporter assay. The effects of miR-142-3p on endothelial apoptosis and atherosclerosis were further analyzed in an in vivo model using ApoE^-/- mice fed with high-fat diet (HFD). Results: MiR-142-3p expression was substantially up-regulated during the ox-LDL-elicited apoptosis in HAECs. Forced expression of miR-142-3p exacerbated apoptosis in ECs whereas inhibition of miR-142-3p could partly alleviate apoptotic cell death mediated by ox-LDL. Further analysis identified Rictor as a direct target of miR-142-3p, and Rictor knockdown abolished the anti-apoptotic effect of miR-142-3p inhibitor. Moreover, the Akt/endothelial nitric oxide synthase (eNOS) signaling pathway was found to mediate the beneficial effect of miR-142-3p inhibitor on endothelial apoptosis. Finally, systemic treatment with miR-142-3p antagomir attenuated endothelial apoptosis and retarded the progression of atherosclerosis in the aorta of ApoE^-/- mice. Conclusions: Down-regulation of miR-142-3p inhibited ECs apoptosis and atherosclerotic development by up-regulating the expression of Rictor and activating the Akt/eNOS signaling pathway. This indicates that miR-142-3p may be a potential target for the prevention and treatment of atherosclerosis.

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MicroRNA-142-3p inhibits hypoxia/reoxygenation-induced apoptosis and fibrosis of cardiomyocytes by targeting high mobility group box 1

Cited by 80 publications

References 31 publications

MiRNA Expression Profile of the Myocardial Tissue of Pigs with Coronary Microembolization

MiRNA Expression Profile of the Myocardial Tissue of Pigs with Coronary Microembolization

MicroRNA-142-3p relieves neuropathic pain by targeting high mobility group box 1

MicroRNA-142-3p Induces Atherosclerosis-Associated Endothelial Cell Apoptosis by Directly Targeting Rictor

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