RGD Reference Report - The role of microRNA-1 targeting of MAPK3 in myocardial ischemia-reperfusion injury in rats undergoing sevoflurane preconditioning via the PI3K/Akt pathway.

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The role of microRNA-1 targeting of MAPK3 in myocardial ischemia-reperfusion injury in rats undergoing sevoflurane preconditioning via the PI3K/Akt pathway.
Authors:	Hao, Yun-Ling Fang, Hong-Cheng Zhao, Hong-Lei Li, Xiao-Li Luo, Ying Wu, Bao-Quan Fu, Ming-Jie Liu, Wei Liang, Jin-Jie Chen, Xie-Hui
Citation:	Hao YL, etal., Am J Physiol Cell Physiol. 2018 Sep 1;315(3):C380-C388. doi: 10.1152/ajpcell.00310.2017. Epub 2018 May 9.
RGD ID:	13800564
Pubmed:	PMID:29741915 (View Abstract at PubMed)
DOI:	DOI:10.1152/ajpcell.00310.2017 (Journal Full-text)
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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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
MAPK3	Human	Myocardial Reperfusion Injury		ISO	Mapk3 (Rattus norvegicus)		RGD
MIR1-2	Human	Myocardial Reperfusion Injury	treatment	ISO	Mir1 (Rattus norvegicus)		RGD
Mapk3	Rat	Myocardial Reperfusion Injury		IEP			RGD
Mapk3	Mouse	Myocardial Reperfusion Injury		ISO	Mapk3 (Rattus norvegicus)		RGD
Mir1	Rat	Myocardial Reperfusion Injury	treatment	IMP			RGD
Mir1a-2	Mouse	Myocardial Reperfusion Injury	treatment	ISO	Mir1 (Rattus norvegicus)		RGD

Objects Annotated

Genes (Rattus norvegicus)

Mapk3 (mitogen activated protein kinase 3)

Mir1 (microRNA 1)

Genes (Mus musculus)

Mapk3 (mitogen-activated protein kinase 3)

Mir1a-2 (microRNA 1a-2)

Genes (Homo sapiens)

MAPK3 (mitogen-activated protein kinase 3)

MIR1-2 (microRNA 1-2)

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