RGD Reference Report - miR-145-5p attenuates inflammatory response and apoptosis in myocardial ischemia-reperfusion injury by inhibiting (NADPH) oxidase homolog 1. - Rat Genome Database

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miR-145-5p attenuates inflammatory response and apoptosis in myocardial ischemia-reperfusion injury by inhibiting (NADPH) oxidase homolog 1.

Authors: Tan, Lili  Liu, Limin  Yao, Jian  Piao, Chenghao 
Citation: Tan L, etal., Exp Anim. 2021 Aug 6;70(3):311-321. doi: 10.1538/expanim.20-0160. Epub 2021 Mar 4.
RGD ID: 329955358
Pubmed: PMID:33658472   (View Abstract at PubMed)
PMCID: PMC8390312   (View Article at PubMed Central)
DOI: DOI:10.1538/expanim.20-0160   (Journal Full-text)

Myocardial ischemia-reperfusion (I/R) injury is a common complication following reperfusion therapy that involves a series of immune or apoptotic reactions. Studies have revealed the potential roles of miRNAs in I/R injury. Herein, we established a myocardial I/R model in rats and a hypoxia/reoxygenation (H/R) model in H9c2 cells and investigated the effect of miR-145-5p on myocardial I/R injury. After 3 h or 24 h of reperfusion, left ventricular end-systolic pressure (LVESP), ejection fraction (EF), and fractional shortening (FS) were obviously decreased, and left ventricular end-diastolic pressure (LVEDP) was increased. Meanwhile, I/R induced an increase in myocardial infarction area. Moreover, a decrease in miR-145-5p and increase in (NADPH) oxidase homolog 1 (NOH-1) were observed following I/R injury. With this in mind, we performed a luciferase reporter assay and demonstrated that miR-145-5p directly bound to NOH-1 3' untranslated region (UTR). Furthermore, miR-145-5p mimics decreased the levels of tumor necrosis factor (TNF)-α, IL-1β, and IL-6 via oxygen and glucose deprivation/reperfusion (OGD/R) stimulation. Upregulation of miR-145-5p increased cell viability and reduced apoptosis accompanied by downregulation of Bax, cleaved caspase-3, cleaved poly(ADP-ribose) polymerase (PARP) and upregulation of Bcl2. In addition, miR-145-5p overexpression increased superoxide dismutase (SOD) activity and reduced reactive oxygen species (ROS) and malondialdehyde (MDA) content under OGD/R stress. Notably, NOH-1 could significantly abrogate the above effects, suggesting that it is involved in miR-145-5p-regulated I/R injury. In summary, our findings indicated that miR-145-5p/NOH-1 has a protective effect on myocardial I/R injury by inhibiting the inflammatory response and apoptosis.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Myocardial Reperfusion Injury  ISOMir145 (Rattus norvegicus)329955358; 329955358RNA:decreased expression:heartRGD 
Myocardial Reperfusion Injury  IEP 329955358RNA:decreased expression:heartRGD 
Myocardial Reperfusion Injury  ISONox1 (Rattus norvegicus)329955358; 329955358mRNA:increased expression:heartRGD 
Myocardial Reperfusion Injury  IEP 329955358mRNA:increased expression:heartRGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir145  (microRNA 145)
Nox1  (NADPH oxidase 1)

Genes (Mus musculus)
Mir145a  (microRNA 145a)
Nox1  (NADPH oxidase 1)

Genes (Homo sapiens)
MIR145  (microRNA 145)
NOX1  (NADPH oxidase 1)


Additional Information