MiR-26a-5p inhibits GSK3β expression and promotes cardiac hypertrophy in vitro

Tang, Liang; Xie, Jianhong; Yu, Xiaoqin; Zheng, Yangyang

doi:10.7717/peerj.10371

Cited by 13 publications

(12 citation statements)

References 42 publications

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“…miR-26a inhibits the development of atherosclerosis by targeting TRPC3 49 , but enhances myocardial damage in myocardial ischemia and reperfusion 50 . miR-26a promotes myocardial fibrosis in acute MI 51 , and enhances autophagy activation in myocardial cells and cardiac hypertrophy by controlling GSK3β 52 . On the other hand, miR-26b relieves inflammation and remodeling in MI mice by suppressing the MAPK pathway 53 and promotes the proliferation, survival, and angiogenesis of endothelial cells 54 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26a/b-5p promotes myocardial infarction-induced cell death by downregulating cytochrome c oxidase 5a

et al. 2021

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Myocardial infarction (MI) damage induces various types of cell death, and persistent ischemia causes cardiac contractile decline. An effective therapeutic strategy is needed to reduce myocardial cell death and induce cardiac recovery. Therefore, studies on molecular and genetic biomarkers of MI, such as microRNAs (miRs), have recently been increasing and attracting attention due to the ideal characteristics of miRs. The aim of the present study was to discover novel causative factors of MI using multiomics-based functional experiments. Through proteomic, MALDI-TOF-MS, RNA sequencing, and network analyses of myocardial infarcted rat hearts and in vitro functional analyses of myocardial cells, we found that cytochrome c oxidase subunit 5a (Cox5a) expression is noticeably decreased in myocardial infarcted rat hearts and myocardial cells under hypoxic conditions, regulates other identified proteins and is closely related to hypoxia-induced cell death. Moreover, using in silico and in vitro analyses, we found that miR-26a-5p and miR-26b-5p (miR-26a/b-5p) may directly modulate Cox5a, which regulates hypoxia-related cell death. The results of this study elucidate the direct molecular mechanisms linking miR-26a/b-5p and Cox5a in cell death induced by oxygen tension, which may contribute to the identification of new therapeutic targets to modulate cardiac function under physiological and pathological conditions.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-26a/b-5p promotes myocardial infarction-induced cell death by downregulating cytochrome c oxidase 5a

et al. 2021

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“…Recently, substantial recognition has been given to plasma miRNAs as possible functional biomarkers that may serve as key post-transcriptional regulators of gene expression networks in various clinical scenarios, including heart failure. Previous studies have shown that many miRNAs were downregulated in cardiac hypertrophy, like miR-101b (Lee et al 2017), miR-1 (Seok et al 2020), and miR-26a-5p (Tang et al 2020), which mitigate the hypertrophic responses. Inversely, the upregulated miRNAs including miR-22 (Huang et al 2013), miR-297 (Bao et al 2017), and miR-217 promoted cardiac hypertrophy and dysfunction (Nie et al 2018).…”

Section: Discussionmentioning

confidence: 97%

MiR-423-5p Inhibition Exerts Protective Effects on Angiotensin II-Induced Cardiomyocyte Hypertrophy

Liu

Gao

et al. 2023

Tohoku J. Exp. Med.

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Angiotensin II (Ang II) is a kind of bioactive peptide, which can contribute to cardiac hypertrophy. MicroRNAs (miRNAs) play critical role in various heart diseases. The cardioprotective effect of miR-423-5p inhibition has been confirmed by previous studies. But its role in cardiac hypertrophy induced by Ang II is unknown. This study focused on the potential of miR-423-5p in cardiomyocyte hypertrophy under the treatment of Ang II. Our results revealed that miR-423-5p expression was upregulated in Ang II-treated human cardiomyocytes (HCMs). Importantly, miR-423-5p knockdown suppressed Ang II-induced cardiomyocyte hypertrophy and oxidative stress in HCMs. Bioinformatics analysis and luciferase reporter assay confirmed that the suppressor of Ty 6 homolog (SUPT6H) was a target gene of miR-423-5p.Interestingly, SUPT6H knockdown aggravated cardiomyocyte hypertrophy and oxidative stress in Ang II-stimulated HCMs, which were then reversed by silenced miR-423-5p. In conclusion, miR-423-5p knockdown exerts its protective effects on Ang IIinduced cardiomyocyte hypertrophy in HCMs via modulating SUPT6H expression.

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“…Interestingly, delivery of miR-29a-3p has a beneficial effect in myocardial injury ( Ren et al, 2021 ) and cardiac hypertrophy ( Xie et al, 2020 ). Similarly, the hsa-mir-26a/b-5p was highly expressed in cardiac hypertrophy ( Tang et al, 2020 ) and promoted myocardial infarction-induced cell death ( Jung et al, 2021 ), yet overexpression of miR-26a/b attenuated cardiac fibrosis ( Tang et al, 2017 ; Wang et al, 2019 ) and alleviated cardiac hypertrophy and dysfunction ( Shi et al, 2021 ). Lastly, the hsa-mir-124-3p was reported to promote cardiac fibroblast activation and proliferation ( Zhu et al, 2021 ), and its inhibition protects against acute myocardial infarction by suppressing cardiomyocyte apoptosis ( Hu et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Long-term culture of patient-derived cardiac organoids recapitulated Duchenne muscular dystrophy cardiomyopathy and disease progression

Marini

Marino

Aliberti

et al. 2022

Front. Cell Dev. Biol.

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Duchenne Muscular Dystrophy (DMD) is an X-linked neuromuscular disease which to date is incurable. The major cause of death is dilated cardiomyopathy however, its pathogenesis is unclear as existing cellular and animal models do not fully recapitulate the human disease phenotypes. In this study, we generated cardiac organoids from patient-derived induced pluripotent stem cells (DMD-COs) and isogenic-corrected controls (DMD-Iso-COs) and studied if DMD-related cardiomyopathy and disease progression occur in the organoids upon long-term culture (up to 93 days). Histological analysis showed that DMD-COs lack initial proliferative capacity, displayed a progressive loss of sarcoglycan localization and high stress in endoplasmic reticulum. Additionally, cardiomyocyte deterioration, fibrosis and aberrant adipogenesis were observed in DMD-COs over time. RNA sequencing analysis confirmed a distinct transcriptomic profile in DMD-COs which was associated with functional enrichment in hypertrophy/dilated cardiomyopathy, arrhythmia, adipogenesis and fibrosis pathways. Moreover, five miRNAs were identified to be crucial in this dysregulated gene network. In conclusion, we generated patient-derived cardiac organoid model that displayed DMD-related cardiomyopathy and disease progression phenotypes in long-term culture. We envision the feasibility to develop a more complex, realistic and reliable in vitro 3D human cardiac-mimics to study DMD-related cardiomyopathies.

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MiR-26a-5p inhibits GSK3β expression and promotes cardiac hypertrophy in vitro

Cited by 13 publications

References 42 publications

MicroRNA-26a/b-5p promotes myocardial infarction-induced cell death by downregulating cytochrome c oxidase 5a

MicroRNA-26a/b-5p promotes myocardial infarction-induced cell death by downregulating cytochrome c oxidase 5a

MiR-423-5p Inhibition Exerts Protective Effects on Angiotensin II-Induced Cardiomyocyte Hypertrophy

Long-term culture of patient-derived cardiac organoids recapitulated Duchenne muscular dystrophy cardiomyopathy and disease progression

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