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Title:
Human umbilical cord bloodāderived MSCs exosome attenuate myocardial injury by inhibiting ferroptosis in acute myocardial infarction mice | Cell Biology and Toxicology
Description:
The exosome of MSCs derived from human umbilical cord blood (HUCB-MSC) has been reported to have cardioprotective effects on mouse models of acute myocardial infarction (AMI) and cardiomyocyte hypoxia injury, but the exact mechanisms involved require further investigation. This paper aimed to study the role of HUCB-MSC-exosomes in inhibiting ferroptosis to attenuate myocardial injury. Compared with sham or normoxia groups, RT-PCR and western blotting showed that divalent metal transporter 1 (DMT1) expression was significantly increased, and Prussian blue staining, ferrous iron (Fe2+), MDA, and GSH level detection demonstrated that ferroptosis occurred in the infraction myocardium and in cardiomyocyte following hypoxia-induced injury. Overexpression of DMT1 promoted H/R-induced myocardial cell ferroptosis, while knockdown of DMT1 significantly inhibited the ferroptosis. HUCB-MSCs-derived exosomes inhibited ferroptosis and reduced myocardial injury, which was abolished in exosome with miR-23a-3p knockout. Moreover, dual luciferase reporter assay confirmed that DMT1 was a target gene of miR-23a-3p. In conclusion, HUCB-MSCs-exosomes may suppress DMT1 expression by miR-23a-3p to inhibit ferroptosis and attenuate myocardial injury.
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article, google, scholar, ferroptosis, myocardial, injury, cell, cells, cas, infarction, wang, iron, stem, dmt, pubmed, human, acute, privacy, cookies, content, data, research, umbilical, cord, exosome, derived, mesenchymal, cardiovascular, central, sci, undefined, henan, esm, png, high, resolution, image, tif, analysis, information, publish, search, attenuate, mice, song, sun, cardiomyocyte, divalent, exosomes, mirap,
Topics {āļø}
stem cells int mir-23a-3p knockout sk-n-sh cells acute myocardial infarction attenuate myocardial injury month download article/chapter hypoxia-induced injury mir-23a-3p cardiomyocyte hypoxia injury focal cerebral ischemia-reperfusion hucb-mscs-exosomes transferrin-bound iron uptake noxious iron-calcium connections reduced myocardial injury breast cancer cells iron-regulatory peptide hepcidin myocardial infarction sulfasalazine-induced ferroptosis related subjects mscs derived article cell biology hucb-msc-exosomes full article pdf microrna regulatory landscape promote colorectal tumorigenesis msc-derived exosomes zhenwei ge privacy choices/manage cookies divalent metal transporter 7a-5p derived extracellular vesicles derived endoplasmic reticulum stress cardiovascular research technology research projects jak-stat3 signaling dmt1 significantly inhibited heart transplantation zg contributed data dexmedetomidine inhibits ferroptosis transferrin regulate ferroptosis hepatic iron accumulation iron-dependent form nonapoptotic cell death ferroptotic cell death european economic area toxicology aims western blotting showed prussian blue staining jacc review topic coding rna h19
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headline:Human umbilical cord bloodāderived MSCs exosome attenuate myocardial injury by inhibiting ferroptosis in acute myocardial infarction mice
description:The exosome of MSCs derived from human umbilical cord blood (HUCB-MSC) has been reported to have cardioprotective effects on mouse models of acute myocardial infarction (AMI) and cardiomyocyte hypoxia injury, but the exact mechanisms involved require further investigation. This paper aimed to study the role of HUCB-MSC-exosomes in inhibiting ferroptosis to attenuate myocardial injury. Compared with sham or normoxia groups, RT-PCR and western blotting showed that divalent metal transporter 1 (DMT1) expression was significantly increased, and Prussian blue staining, ferrous iron (Fe2+), MDA, and GSH level detection demonstrated that ferroptosis occurred in the infraction myocardium and in cardiomyocyte following hypoxia-induced injury. Overexpression of DMT1 promoted H/R-induced myocardial cell ferroptosis, while knockdown of DMT1 significantly inhibited the ferroptosis. HUCB-MSCs-derived exosomes inhibited ferroptosis and reduced myocardial injury, which was abolished in exosome with miR-23a-3p knockout. Moreover, dual luciferase reporter assay confirmed that DMT1 was a target gene of miR-23a-3p. In conclusion, HUCB-MSCs-exosomes may suppress DMT1 expression by miR-23a-3p to inhibit ferroptosis and attenuate myocardial injury.
datePublished:2020-06-13T00:00:00Z
dateModified:2020-06-13T00:00:00Z
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HUCB-MSCs
Exosome
MiR-23a-3p
Acute myocardial infarction
Ferroptosis
Cell Biology
Pharmacology/Toxicology
Biochemistry
general
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headline:Human umbilical cord bloodāderived MSCs exosome attenuate myocardial injury by inhibiting ferroptosis in acute myocardial infarction mice
description:The exosome of MSCs derived from human umbilical cord blood (HUCB-MSC) has been reported to have cardioprotective effects on mouse models of acute myocardial infarction (AMI) and cardiomyocyte hypoxia injury, but the exact mechanisms involved require further investigation. This paper aimed to study the role of HUCB-MSC-exosomes in inhibiting ferroptosis to attenuate myocardial injury. Compared with sham or normoxia groups, RT-PCR and western blotting showed that divalent metal transporter 1 (DMT1) expression was significantly increased, and Prussian blue staining, ferrous iron (Fe2+), MDA, and GSH level detection demonstrated that ferroptosis occurred in the infraction myocardium and in cardiomyocyte following hypoxia-induced injury. Overexpression of DMT1 promoted H/R-induced myocardial cell ferroptosis, while knockdown of DMT1 significantly inhibited the ferroptosis. HUCB-MSCs-derived exosomes inhibited ferroptosis and reduced myocardial injury, which was abolished in exosome with miR-23a-3p knockout. Moreover, dual luciferase reporter assay confirmed that DMT1 was a target gene of miR-23a-3p. In conclusion, HUCB-MSCs-exosomes may suppress DMT1 expression by miR-23a-3p to inhibit ferroptosis and attenuate myocardial injury.
datePublished:2020-06-13T00:00:00Z
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MiR-23a-3p
Acute myocardial infarction
Ferroptosis
Cell Biology
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