LncRNA 1700020I14Rik/miR-297a/CGRP axis suppresses myocardial cell apoptosis in myocardial ischemia-reperfusion injury

2020 ◽  
Vol 122 ◽  
pp. 54-61
Author(s):  
Fudong Hu ◽  
Jinhua Yang ◽  
Xi Chen ◽  
Yangyang Shen ◽  
Kui Chen ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Cell ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

scholarly journals microRNA-30c promotes myocardial ischemia reperfusion injury by activating SIRT1 mediating NF-κB pathway

2019 ◽  
Author(s):  
Jianfeng Chen ◽  
Shufeng Xue ◽  
Mingming Zhang ◽  
Junlong Wu ◽  
Shouyan Zhang
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Cell ◽  
Injury Model ◽  
Tnf Α ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Background This study aimed to investigate the effect of miR-30c on myocardial ischemia reperfusion (IR) injury and its underlying molecular mechanisms.Methods In our study, rat myocardial IR injury model was established and hemodynamic examination was performed. Moreover, the myocardial infarct size was detected by TTC staining. The pathologic change of myocardial tissues was measured by HE staining. The myocardial cell apoptosis was measured by TUNEL staining and flow cytometry. The expression of miR-30c and Sirtuin 1 (SIRT1) was detected by qRT-PCR. The levels of IL-1β, IL-6 and TNF-α were detected by ELISA. The expressions of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 were detected by western blot. The luciferase activity was measured by dual luciferase reporter gene assay. Interaction between miR-30c and SIRT1 were analyzed by RNA immunoprecipitation assay.Results Our results showed that rat myocardial IR injury model was successfully established and IR injury induced myocardial injury in rats. miR-30c increased the levels of IL-1β, IL-6 and TNF-α and myocardial cell apoptosis by activating NF-κB pathway. In addition, we also confirmed that SIRT1 was the target gene of miR-30c. SIRT1 could reverse the effect of miR-30c on the process of inflammation and apoptosis, as well as the activation of NF-κB pathway in myocardial cells.Conclusions Our study demonstrated that miR-30c could promote myocardial ischemia reperfusion injury through activating SIRT1 mediating NF-κB pathway.

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

2018 ◽  
Vol 51 (1) ◽  
pp. 46-62 ◽  
Author(s):  
Hong Tan ◽  
Jie Qi ◽  
Bo-Yuan Fan ◽  
Jian Zhang ◽  
Fei-Fei Su ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Mouse Model ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Infarct Area ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Background/Aims: This study was developed to investigate a potential therapeutic method for myocardial ischemia/reperfusion injury involving the promotion of miR-24-3p expression. Methods: Microarray analysis was used to screen differentially expressed genes in a myocardial ischemia/reperfusion (I/R) injury mouse model. Gene set enrichment analysis was utilized to determine vital signaling pathways. Targeting verification was conducted with a luciferase reporter assay. Myocardial I/R injury was developed in mice, and the expression levels of RIPK1 and miR-24-3p were investigated by qRT-PCR and Western blot. Hemodynamic parameters and the activity of serum myocardial enzymes were measured to evaluate cardiac function. Infarct area was observed through HE and TTC staining. Myocardial cell apoptosis was examined by TUNEL staining and caspase-3 activity analysis. Results: RIPK1 was an upregulated mRNA found by microarray analysis and a verified target of the downregulated miRNA miR-24-3p. The upregulation of RIPK1 (1.8-fold) and the downregulation of miR-24-3p (0.3-fold) were confirmed in I/R mice. RIPK1 led to impaired cardiac function indexes, increased infarct area and cell apoptosis, while miR-24-3p could reverse the injury by regulating RIPK1. The TNF signaling pathway was proven to be involved in myocardial I/R injury through the detection of the dysregulation of related proteins. Conclusion: In conclusion, RIPK1 was upregulated and miR-24-3p was downregulated in a myocardial I/R injury mouse model. RIPK1 could aggravate myocardial I/R injury via the TNF signaling pathway, while miR-24-3p could suppress RIPK1 and therefore exert cardioprotective effects in myocardial I/R injury.

scholarly journals The role of microRNA-1 targeting of MAPK3 in myocardial ischemia-reperfusion injury in rats undergoing sevoflurane preconditioning via the PI3K/Akt pathway

2018 ◽  
Vol 315 (3) ◽  
pp. C380-C388 ◽  
Author(s):  
Yun-Ling Hao ◽  
Hong-Cheng Fang ◽  
Hong-Lei Zhao ◽  
Xiao-Li Li ◽  
Ying Luo ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Akt Pathway ◽  
Area At Risk ◽  
Sevoflurane Preconditioning ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Recent studies have uncovered the vital roles played by microRNAs in regulating cardiac injury. Among them, the cardiac enriched microRNA-1 (miR-1) has been extensively studied and proven to be detrimental to cardiac myocytes. Hence, the current study aimed to explore whether miR-1 affects myocardial ischemia-reperfusion injury (MIRI) in rats undergoing sevoflurane preconditioning and the underlying mechanism. After successful model establishment, rats with MIRI were transfected with mimics or inhibitors of miR-1, or siRNA against MAPK3, and then were injected with sevoflurane. A luciferase reporter gene assay was conducted to evaluate the targeting relationship between miR-1 and MAPK3. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were employed to evaluate the expressions of miR-1, MAPK3, phosphatidylinositol 3-kinase (PI3K), and Akt. Additionally, the concentration of lactate dehydrogenase (LDH) was determined. Cell apoptosis and viability were assessed using TUNEL and cell counting kit-8 assays, and the ischemic area at risk and infarct size were detected using Evans blue and triphenyltetrazolium chloride staining. MAPK3 was found to be the target gene of miR-1. miR-1 expressed at a high level whereas MAPK3 expressed at a low level in MIRI rats. Overexpressing miR-1 or silencing MAPK3 blocked the PI3K/Akt pathway to increase cell apoptosis, ischemic area at risk, and infarct area but decreased cell viability and increased LDH concentration. In contrast, miR-1 downregulation abrogated the effects induced by miR-1 mimics or siRNA against MAPK3. These findings indicate that inhibition of miR-1 promotes MAPK3 to protect against MIRI in rats undergoing sevoflurane preconditioning through activation of the PI3K/Akt pathway.

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