MicroRNA-24-3p Attenuates Myocardial Ischemia/Reperfusion Injury by Suppressing RIPK1 Expression in Mice

Tan, Hong; Qi, Jie; Fan, Boyuan; Zhang, Jian; Su, Feifei; Wang, Hong-Tao

doi:10.1159/000495161

Cited by 72 publications

(48 citation statements)

References 23 publications

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“…riPK1 is a crucial regulator of TnFr1 signaling (17). it has been reported that riPK1 is a target gene of mir-24-3p (36). in the present study, it was demonstrated by the dual-luciferase reporter assay that riPK1 is a target of mir-421.…”

Section: Discussionsupporting

confidence: 62%

microRNA‑421 participates in vitiligo development through regulating human melanocyte survival by targeting receptor‑interacting serine/threonine kinase 1

et al. 2019

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Vitiligo is a common localized or generalized skin pigmentation disorder. endoplasmic reticulum (er) stress may be implicated in the development of vitiligo. microrna-421 (mir-421) has been reported to be dysregulated in various human tumors. However, there is no report to date on the role of mir-421 in vitiligo development. The present study demonstrated that 3 µM tunicamycin (TM) increased the expression of the er stress-related proteins protein kinase rna-like endoplasmic reticulum kinase (PerK), α subunit of eukaryotic translation initiation factor 2 (eiF2α) and c/eBP homologous protein (cHoP) in human primary epidermal melanocytes. Moreover, TM suppressed melanocyte viability and induced apoptosis. reverse transcription-quantitative Pcr analysis demonstrated that TM promoted mir-421 expression in human melanocytes. next, TargetScan and dual luciferase reporter gene assay indicated that receptor-interacting serine/threonine kinase 1 (riPK1) was a direct target of mir-421. riPK1 expression was significantly downregulated in TM-induced human melanocytes. Subsequently, the effect of mir-421 downregulation on the damage of human melanocytes induced by er stress was investigated. Human melanocytes were transfected with inhibitor control, mir-421 inhibitor, mir-421 inhibitor + control-short hairpin (sh)rna, or mir-421 inhibitor + riPK1-shrna for 24 h and then treated with TM (3 µM) for 48 h. TM was found to upregulate PerK, eiF2α and cHoP protein expression in human melanocytes, which was reduced by an mir-421 inhibitor. in addition, the mir-421 inhibitor increased viability and reduced apoptosis in TM-treated melanocytes. Furthermore, all these effects of the mir-421 inhibitor on TM-induced human melanocytes were reversed by riPK1-shrna. Further analyses revealed that the mir-421 inhibitor activated the phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin signaling pathway in TM-induced human melanocytes. These data collectively suggest that mir-421 may serve as a new treatment target in vitiligo development.

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Section: Discussionsupporting

confidence: 62%

microRNA‑421 participates in vitiligo development through regulating human melanocyte survival by targeting receptor‑interacting serine/threonine kinase 1

et al. 2019

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“…miRNAs participate in the regulation of various biological processes, including cell proliferation, cell cycle progression, and cell survival . There is some evidence to suggest that miRNA expression changed the across different species from miRNAs in many models of myocardial I/R injury, demonstrating the pivotal role of miRNAs in myocardial ischemic injury . It has been proposed that miR‐27 regulates cell differentiation in many diseases .…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, we concluded that the miR-27 reduction may be caused by (Figure 2A 17 There is some evidence to suggest that miRNA expression changed the across different species from miRNAs in many models of myocardial I/R injury, demonstrating the pivotal role of miRNAs in myocardial ischemic injury. 1,18 It has been proposed that miR-27 regulates cell differentiation in many diseases. 19,20 It has conclusively been shown that miR-27 may be involved in occurrence and development of atherosclerosis.…”

Section: Downregulated Expression Of Mir-27 In Myocardial Ischemia mentioning

confidence: 99%

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MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Zhang

2019

The Kaohsiung J of Med Scie

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MiR‐27 prevents atherosclerosis by inhibiting inflammatory responses induced by lipoprotein lipase. Overexpression of miR‐27b attenuates angiotensin‐induced atrial fibrosis. Nevertheless, studies have rarely investigated on the effect of miR‐27 in cardiomyocyte injury. H9c2 cells were transfected with miR‐27 mimic/inhibitor. Then the cell proliferation was tested by MTT assay and the cell apoptosis was detected by flow cytometry. The luciferase activity assay was utilized to analyze the relationship between miR‐27 and TGFBR1. Quantificational real‐time polymerase chain reaction and western blot were utilized to detect the cardiomyocyte differentiation marker and nuclear factor kappa B (NF‐κB) pathway. Our outcomes demonstrated that miR‐27 expression was downregulated cardiomyocyte injury subjected to hypoxia/reoxygenation (H/R). Additionally, overexpression of miR‐27 could significantly alleviate cardiomyocyte injury by regulating cell activity and apoptosis. The luciferase activity assay confirmed that transforming growth factor ß receptor 1 (TGFBR1) is a direct hallmark of miR‐27. Besides, overexpression of miR‐27 promoted the expression of TGFBR1 in H/R model. After transfection with miR‐27 mimic/inhibitor, the expression of NF‐κB pathway‐related proteins was decreased/increased. Taken together, our data manifested that miR‐27 repressed cardiomyocyte injury induced by H/R via mediating TGFBR1 and inhibiting NF‐κB signaling pathway. Furthermore, miR‐27/ TGFBR1 might be utilized as hopeful biomarkers for myocardial ischemia diagnosis and treatment.

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“…Asymptomatic carotid stenosis [63], familial hypercholesterolemia and coronary artery disease [64], angina pectoris [65], ischemic dilated cardiomyopathy [66], small and large abdominal aortic aneurysm [61], myocardial ischemia/reperfusion [67,68], diabetes mellitus [14,24,52,54] hsa-miR-26a-5p 3p22.2 12q14.1 [69] Heart failure, cardiac hypertrophy [70], myocardial infarction [51,71,72], ischemia/reperfusion injury [73], pulmonary arterial hypertension [74], T1DM [75], diabetic nephropathy [57] hsa-miR-29a-3p 7q32.3…”

Section: Introductionmentioning

confidence: 99%

Diabetes Mellitus and Cardiovascular Risk Assessment in Mothers with a History of Gestational Diabetes Mellitus Based on Postpartal Expression Profile of MicroRNAs Associated with Diabetes Mellitus and Cardiovascular and Cerebrovascular Diseases

Hromadníková

Dvořáková

Krofta

2020

IJMS

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Mothers with a history of gestational diabetes mellitus (GDM) have an increased risk of developing diabetes in the future and a lifelong cardiovascular risk. Postpartal expression profile of cardiovascular/cerebrovascular disease associated microRNAs was assessed 3–11 years after the delivery in whole peripheral blood of young and middle-aged mothers with a prior exposure to GDM with the aim to identify a high-risk group of mothers at risk of later development of diabetes mellitus and cardiovascular/cerebrovascular diseases who would benefit from implementation of early primary prevention strategies and long-term follow-up. The hypothesis of the assessment of cardiovascular risk in women was based on the knowledge that a series of microRNAs play a role in the pathogenesis of diabetes mellitus and cardiovascular/cerebrovascular diseases. Abnormal expression profile of multiple microRNAs was found in women with a prior exposure to GDM (miR-1-3p, miR-16-5p, miR-17-5p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23a-3p, miR-24-3p, miR-26a-5p, miR-29a-3p, miR-100-5p, miR-103a-3p, miR-125b-5p, miR-126-3p, miR-130b-3p, miR-133a-3p, miR-143-3p, miR-145-5p, miR-146a-5p, miR-181a-5p, miR-195-5p, miR-199a-5p, miR-221-3p, miR-342-3p, miR-499a-5p, and-miR-574-3p). Postpartal combined screening of miR-1-3p, miR-16-5p, miR-17-5p, miR-20b-5p, miR-21-5p, miR-23a-3p, miR-26a-5p, miR-29a-3p, miR-103a-3p, miR-133a-3p, miR-146a-5p, miR-181a-5p, miR-195-5p, miR-199a-5p, miR-221-3p, and miR-499a-5p showed the highest accuracy for the identification of mothers with a prior exposure to GDM at a higher risk of later development of cardiovascular/cerebrovascular diseases (AUC 0.900, p < 0.001, sensitivity 77.48%, specificity 93.26%, cut off >0.611270413). It was able to identify 77.48% mothers with an increased cardiovascular risk at 10.0% FPR. Any of changes in epigenome (upregulation of miR-16-5p, miR-17-5p, miR-29a-3p, and miR-195-5p) that were induced by GDM-complicated pregnancy are long-acting and may predispose mothers affected with GDM to later development of diabetes mellitus and cardiovascular/cerebrovascular diseases. In addition, novel epigenetic changes (upregulation of serious of microRNAs) appeared in a proportion of women that were exposed to GDM throughout the postpartal life. Likewise, a previous occurrence of either GH, PE, and/or FGR, as well as a previous occurrence of GDM, is associated with the upregulation of miR-1-3p, miR-17-5p, miR-20a-5p, miR-20b-5p, miR-29a-3p, miR-100-5p, miR-125b-5p, miR-126-3p, miR-130b-3p, miR-133a-3p, miR-143-3p, miR-145-5p, miR-146a-5p, miR-181a-5p, miR-199a-5p, miR-221-3p, and miR-499a-5p. On the other hand, upregulation of miR-16-5p, miR-21-5p, miR-23a-3p, miR-24-3p, miR-26a-5p, miR-103a-3p, miR-195-5p, miR-342-3p, and miR-574-3p represents a unique feature of aberrant expression profile of women with a prior exposure to GDM. Screening of particular microRNAs may stratify a high-risk group of mothers with a history of GDM who might benefit from implementation of early primary prevention strategies.

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MicroRNA-24-3p Attenuates Myocardial Ischemia/Reperfusion Injury by Suppressing RIPK1 Expression in Mice

Cited by 72 publications

References 23 publications

microRNA‑421 participates in vitiligo development through regulating human melanocyte survival by targeting receptor‑interacting serine/threonine kinase 1

microRNA‑421 participates in vitiligo development through regulating human melanocyte survival by targeting receptor‑interacting serine/threonine kinase 1

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Diabetes Mellitus and Cardiovascular Risk Assessment in Mothers with a History of Gestational Diabetes Mellitus Based on Postpartal Expression Profile of MicroRNAs Associated with Diabetes Mellitus and Cardiovascular and Cerebrovascular Diseases

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