<scp>MiR</scp>‐129‐5p alleviates myocardial injury by targeting suppressor of cytokine signaling 2 after ischemia/reperfusion

Ma, Rui; Chen, Xin; Ma, Yue; Bai, Gang; Li, Dongsheng

doi:10.1002/kjm2.12211

Cited by 12 publications

(8 citation statements)

References 31 publications

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“…More importantly, overexpression of miR-129-5p ameliorated myocardial I/R injury. Consistent with our study, miR-129-5p alleviates myocardial injury after ischemia/reperfusion ( 17 ). miR-129-5p ameliorated ischemia-reperfusion injury by targeting HMGB1 in myocardium ( 18 ).…”

Section: Discussionsupporting

confidence: 92%

Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p

Wei¹,

Zhang²,

Liao³

2022

ijph

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Background: LncRNA FGD5-AS1 regulates the pathogenesis of many human diseases. We aimed to elucidate the function of lncRNA FGD5-AS1 and the regulatory mechanism of lncRNA FGD5-AS1/miR-129-5p in myocardial ischemia-reperfusion (I/R) injury. Methods: Myocardial I/R injury mice model and H/R treated H9c2 cells were established. RT-qPCR and Western blot analysis were used to detect the mRNA and protein expression. Cell viability was detected by MTT assay. Dual luciferase reporter assay was applied to confirm the relationship between lncRNA FGD5-AS1 and miR-129-5p. Results: LncRNA FGD5-AS1 was upregulated in myocardial I/R injury mice models and H/R treated H9c2 cells. Functionally, knockdown of lncRNA FGD5-AS1 promoted cell viability and inhibited apoptosis in H/R treated H9c2 cells. In addition, lncRNA FGD5-AS1 directly targets miR-129-5p. Upregulation of lncRNA FGD5-AS1 weakened the protective effect of miR-129-5p on myocardial I/R injury. Conclusion: LncRNA FGD5-AS1 aggravates myocardial I/R injury by downregulating miR-129-5p.

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Section: Discussionsupporting

confidence: 92%

Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p

Wei¹,

Zhang²,

Liao³

2022

ijph

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“…12 Similarly, miR-129-5p is downregulated in a mouse myocardial I/R model, and miR-129-5p overexpression can alleviate myocardial injury as evidenced by reduced LDH leakage and decreased infract size. 21 Besides, miR-129-5p also represses hydrogen peroxide-induced autophagy and apoptosis in H9c2 cells. 22 Therefore, miR-129-5p can protect H9c2 cardiac myoblasts from H/R injury by reducing myocardial apoptosis and improving cell viability of cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

MiR-129-5p Protects H9c2 Cardiac Myoblasts From Hypoxia/Reoxygenation Injury by Targeting TRPM7 and Inhibiting NLRP3 Inflammasome Activation

Liu

Liao

et al. 2021

Journal of Cardiovascular Pharmacology

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As a biomarker for heart failure, miR-129-5p is abnormally expressed during myocardial I/R, but its specific functions and mechanisms remain largely unclear. Thus, this study explored the roles and possible mechanisms of miR-129-5p in hypoxia/reoxygenation (H/R)-insulted H9c2 cardiac myoblasts. After H/R insult, miR-129-5p expression levels were decreased, along with reduced cell viability and enhanced lactate dehydrogenase release in H9c2 cells. Overexpression of miR-129-5p through transfection of miR-129-5p mimics effectively improved cell viability and reduced lactate dehydrogenase release in H9c2 cells exposed to H/R, along with decreased apoptosis and caspase-3 activities. Moreover, miR-129-5p mimics inhibited reactive oxygen species production and upsurged superoxide dismutase activity in H9c2 cells exposed to H/R, and suppressed H/R-caused massive release of proinflammatory cytokines TNF-a and IL-1b. TRPM7 was identified as the target of miR-129-5p and was negatively regulated by miR-129-5p. TRPM7 overexpression counteracted the antagonistic effect of miR-129-5p on H/R-induced increase in intracellular calcium levels. TRPM7 overexpression also abolished miR-129-5p-induced elevation on cell viability and reduction on apoptosis as well as attenuated miR-129-5p-induced inhibition on reactive oxygen species and IL-1b production. Besides, H/R-induced NLRP3 inflammasome activation was inhibited by miR-129-5p mimic but reactivated by TRPM7. In conclusion, miR-129-5p alleviates H/R injury of H9c2 cardiomyocytes by targeting TRPM7 and inhibiting NLRP3 inflammasome activation, suggesting that miR-129-5p and TRPM7 may be potential therapeutic targets for myocardial I/R injury.

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“…This finding is consistent with previous reports and indicates the reliability of the microarray results in the present study. However, miR-129 was selected for further investigation as it exhibited the most statistically significant difference between the two groups and as previous studies have discussed the role of miR-129 in regulating injury and inflammatory response in different organ injury models ( 19 , 38 , 39 ).…”

Section: Resultsmentioning

confidence: 99%

“…For example, Yang et al ( 54 ) demonstrated that miR-129 overexpression improved neurological function by reducing tissue loss and cell apoptosis in a rat spinal cord injury model. Furthermore, Zeng et al ( 18 ) found that the upregulation of miR-129 reduced nerve injury and inflammatory response in rats with Alzheimer's disease via the downregulation of SOX6, and Ma et al ( 38 ) reported that miR-129 alleviated myocardial injury induced by I/R both under in vitro and in vivo conditions by targeting suppressor of cytokine signaling 2. Chen et al ( 19 ) also found that miR-129 played a protective role in myocardial I/R injury by regulating HMGB1 expression.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑129 plays a protective role in sepsis‑induced acute lung injury through the suppression of pulmonary inflammation via the modulation of the TAK1/NF‑κB pathway

et al. 2021

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Excessive inflammatory response and apoptosis play key roles in the pathogenic mechanisms of sepsis-induced acute lung injury (ALI); however, the molecular pathways linked to ALI pathogenesis remain unclear. Recently, microRNAs (miRNAs/miRs) have emerged as important regulators of inflammation and apoptosis in sepsis-induced ALI; however, the exact regulatory mechanisms of miRNAs remain poorly understood. In the present study, the gene microarray dataset GSE133733 obtained from the Gene Expression Omnibus database was analyzed and a total of 38 differentially regulated miRNAs were identified, including 17 upregulated miRNAs and 21 downregulated miRNAs, in mice with lipopolysaccharide (LPS)-induced ALI, in comparison to the normal control mice. miR-129 was found to be the most significant miRNA, among the identified miRNAs. The upregulation of miR-129 markedly alleviated LPS-induced lung injury, as indicated by the decrease in lung permeability in and the wet-to-dry lung weight ratio, as well as the improved survival rate of mice with ALI administered miR-129 mimic. Moreover, the upregulation of miR-129 reduced pulmonary inflammation and apoptosis in mice with ALI. Of note, transforming growth factor activated kinase-1 (TAK1), a well-known regulator of the nuclear factor-κB (NF-κB) pathway, was directly targeted by miR-129 in RAW 264.7 cells. More importantly, miR-129 upregulation impeded the LPS-induced activation of the TAK1/NF-κB signaling pathway, as illustrated by the suppression of the nuclear phosphorylated-p65, p-IκB-α and p-IKKβ expression levels. Collectively, the findings of the present study indicate that miR-129 protects mice against sepsis-induced ALI by suppressing pulmonary inflammation and apoptosis through the regulation of the TAK1/NF-κB signaling pathway. This introduces the basis for future research concerning the application of miR-129 and its targets for the treatment of ALI.

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MiR‐129‐5p alleviates myocardial injury by targeting suppressor of cytokine signaling 2 after ischemia/reperfusion

Cited by 12 publications

References 31 publications

Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p

Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p

MiR-129-5p Protects H9c2 Cardiac Myoblasts From Hypoxia/Reoxygenation Injury by Targeting TRPM7 and Inhibiting NLRP3 Inflammasome Activation

MicroRNA‑129 plays a protective role in sepsis‑induced acute lung injury through the suppression of pulmonary inflammation via the modulation of the TAK1/NF‑κB pathway

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