MiR-324/SOCS3 Axis Protects Against Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury and Regulates Myocardial Ischemia via TNF/NF-κB Signaling Pathway

Han, Xiao; Chen, Xi; Han, Jiaqi; Zhong, Yu; Li, Qinghua; An, Yi

doi:10.1536/ihj.19-687

Cited by 13 publications

(9 citation statements)

References 72 publications

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“…Inhibition of IL-17 signaling pathway can improve immune response balance and attain cardioprotection in rats with heart failure [ 25 ]. MIR-324/SOCS3 axis can regulate TNF signaling pathway and further improve the hypoxia/reoxygenation-induced myocardial injury [ 26 ]. Study finds that d-Limonene alleviates myocardial infarction injury via antioxidant effect [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Exploration of the molecular targets and mechanisms of suxiao xintong dropping pills for myocardial infarction by network pharmacology method

Chen

et al. 2021

Bioscience Reports

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Background: Suxiao Xintong dropping pills (SXXTDP), a traditional Chinese medicine, is widely applied for treating myocardial infarction (MI). However, its therapy mechanisms are still unclear. Therefore, this research is designed to explore the molecular mechanisms of SXXTDP in treating MI. Methods: The active ingredients of SXXTDP and their corresponding genes of the active ingredients were retrieved from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. MI-related genes were identified via analyzing the expression profiling data (accession number: GSE97320). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed to study the shared genes of drug and disease. Through protein-protein interaction (PPI) network and the Cytoscape plugin cytoHubba, the hub genes were screened out. The compounds and hub targets binding were simulated through molecular docking method. Results: We obtained 21 active compounds and 253 corresponding target genes from TCMSP database. 1833 MI-related genes were identified according to P＜0.05 and |log2FC| ≥ 0.5. 27 overlapping genes between drug and disease were acquired. GO analysis indicated that overlapping genes were mainly enriched in MAP kinase activity and antioxidant activity. KEGG analysis indicated that overlapping genes were mainly enriched in IL-17 signaling pathway and TNF signaling pathway. We obtained 10 hub genes via cytoHubba plugin. Six of the 10 hub genes, including PTGS2, MAPK14, MMP9, MAPK1, NFKBIA, and CASP8, were acted on molecular docking verification with their corresponding compounds of SXXTDP. Conclusion: SXXTDP may exert cardioprotection effect through regulating multiple targets and multiple pathways in MI.

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Section: Discussionmentioning

confidence: 99%

Exploration of the molecular targets and mechanisms of suxiao xintong dropping pills for myocardial infarction by network pharmacology method

Chen

et al. 2021

Bioscience Reports

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“…miR-324-5p overexpression could efficiently alleviate angiogenesis and pernicious cell expansion, eventually decelerating pulmonary arterial hypertension ( 47 ). On the other hand, miR-324 relieved cardiomyocyte damage and oxidative stress of myocardial injury triggered by hypoxia/reoxygenation ( 13 ). Surprisingly, Huang and his colleagues ( 48 ) reported that miR-324-5p activation attenuated apoptosis and ventricular cardiomyocyte injury exacerbated by myocardial ischemia-reperfusion to relieve MI.…”

Section: Discussionmentioning

confidence: 99%

“…miRs are deemed as reliable biomarkers of MI as they regulate downstream genes or axis and affect myocardial function ( 12 ). miR-324 is downregulated in cardiomyocytes with hypoxia/reoxygenation-induced injury, inhibiting cell proliferation ( 13 ). However, research about the specific function of miR-324-5p in MI progression is elusive.…”

Section: Introductionmentioning

confidence: 99%

Role of miRNA-324-5p-Modified Adipose-Derived Stem Cells in Post-Myocardial Infarction Repair

Zhou¹,

Wang²,

Tong³

2021

IJSC

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Background and Objectives: To seek out the role of mircoRNA (miR)-324-5p-modified adipose-derived stem cells (ADSCs) in post-myocardial infarction (MI) myocardial repair. Methods and Results: Rat ADSCs were cultivated and then identified by morphologic observation, osteogenesis and adipogenesis induction assays and flow cytometry. Afterwards, ADSCs were modified by miR-324-5p lentiviral vector, with ADSC proliferation and migration measured. Then, rat MI model was established, which was treated by ADSCs or miR-324-5p-modified ADSCs. Subsequently, the function of miR-324-5p-modified ADSCs in myocardial repair of MI rats was assessed through functional assays. Next, the binding relation of miR-324-5p and Toll-interacting protein (TOLLIP) was validated. Eventually, functional rescue assay of TOLLIP was performed to verify the role of TOLLIP in MI. First, rat ADSCs were harvested. Overexpressed miR-324-5p improved ADSC viability. ADSC transplantation moderately enhanced cardiac function of MI rats, reduced enzyme levels and decreased infarct size and apoptosis; while miR-324-5p-modified ADSCs could better promote post-MI repair. Mechanically, miR-324-5p targeted TOLLIP in myocardial tissues. Moreover, TOLLIP overexpression debilitated the promotive role of miR-324-5p-modified ADSCs in post-MI repair in rats. Conclusions: miR-324-5p-modified ADSCs evidently strengthened post-MI myocardial repair by targeting TOLLIP in myocardial tissues.

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“…One of the genes, SOCS3, was significantly elevated in the MI group ( 52 ). Next, it was confirmed by bioinformatics prediction and luciferase reporter assays that miR-324 was its upstream regulatory miRNA, which could both bind to inhibit SOCS3 expression.…”

Section: Characterization Of Cardiomyocyte Proliferationmentioning

confidence: 99%

“…In in vitro experiments, it was clear that miR-324 overexpression promoted cardiomyocyte proliferation, protected cells from apoptosis in the H/R model, and reduced cardiomyocytes, such as TNF-α, p-p65, and p-IκBα. Thus, it showed that miR-324 might improve cardiomyocyte H/R injury by regulating NFκB ( 52 ).…”

Section: Characterization Of Cardiomyocyte Proliferationmentioning

confidence: 99%

Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration

Qin

Xie

Tang

et al. 2022

Front. Cardiovasc. Med.

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Cardiovascular diseases remain the leading cause of death worldwide, particularly ischemic heart disease (IHD). It is also classified as incurable given the irreversible damage it causes to cardiomyocytes. Thus, myocardial tissue rejuvenation following ischemia is one of the global primary research concerns for scientists. Interestingly, the mammalian heart thrives after an injury during the embryonic or neonatal period; however, this ability disappears with increasing age. Previous studies have found that specific non-coding (nc) RNAs play a pivotal role in this process. Hence, the review herein summarizes the research on cardiomyocyte regenerative medicine in recent years and sets forth the biological functions and mechanisms of the micro (mi)RNA, long non-coding (lnc)RNA, and circular (circ)RNA in the posttranscriptional regulation of cardiomyocytes. In addition, this review summarizes the roles of ncRNAs in specific species while enumerating potential therapeutic strategies for myocardial infarction.

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MiR-324/SOCS3 Axis Protects Against Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury and Regulates Myocardial Ischemia via TNF/NF-κB Signaling Pathway

Cited by 13 publications

References 72 publications

Exploration of the molecular targets and mechanisms of suxiao xintong dropping pills for myocardial infarction by network pharmacology method

Exploration of the molecular targets and mechanisms of suxiao xintong dropping pills for myocardial infarction by network pharmacology method

Role of miRNA-324-5p-Modified Adipose-Derived Stem Cells in Post-Myocardial Infarction Repair

Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration

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