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1.
Front Cardiovasc Med ; 9: 947721, 2022.
Article in English | MEDLINE | ID: mdl-36330017

ABSTRACT

Background: Cardiovascular disease, including acute myocardial infarction (AMI), is a major global cause of mortality and morbidity. Specificity and sensitivity limit the utility of classic diagnostic biomarkers for AMI. Therefore, it is critical to identify novel biomarkers for its accurate diagnosis. Cumulative studies have demonstrated that circulating microRNAs (miRs) participate in the pathophysiological processes of AMI and are promising diagnostic biomarkers for the condition. This study aimed to ascertain the diagnostic accuracy of circulating miR-21-5p and miR-126 used as biomarkers in patients with AMI and infarct-related artery total occlusion (IR-ATO) or infarct-related blood-vessel recanalization (IR-BVR). Methods: The expression of miR-21-5p and miR-126 was examined separately in 50 healthy subjects, 51 patients with IR-ATO AMI, and 49 patients with IR-BVR AMI using quantitative real-time polymerase chain reaction. Results: When compared with the control group, the IR-ATO AMI group exhibited increased miR-21-5p (p < 0.0001) and miR-126 (p < 0.0001), and the IR-BVR AMI group exhibited increased miR-21-5p (p < 0.0001). However, there was no significant difference in miR-126 between the IR-BVR AMI and the control groups. A Spearman's correlation coefficient showed a strong correlation was found between miR-21-5p, miR-126, cardiac troponin-I, and creatine kinase isoenzyme in all three groups, while a receiver operating characteristic analysis revealed that miR-21-5p and miR-126 exhibited considerable diagnostic accuracy for IR-ATO AMI. Conclusion: Circulating miR-21-5p and miR-126 may be promising prognostic biomarkers for patients with AMI and IR-ATO.

2.
Int J Mol Med ; 45(5): 1591-1600, 2020 May.
Article in English | MEDLINE | ID: mdl-32323745

ABSTRACT

Adipose tissue­derived stem cells (ASCs) are beneficial for myocardial regeneration. The physiological oxygen content of human organs is estimated to range between 1 and 11%. However, in the majority of previous in vitro studies with cultured ASCs, the O2 concentration was artificially set to 21%. The present study aimed to compare the protective effects of rat ASCs on neonatal rat ventricular myocytes (NRVMs) under normoxic (21% O2) and physioxic (5% O2) conditions. Rat NRVMs cultured under normoxia or physioxia were treated with H2O2 or left untreated, and further co­cultured with ASCs in 21% or 5% O2. The apoptosis of NRVMs was evaluated by Annexin V staining and quantitating the protein levels of Bcl­2 and Bax by western blotting. The oxidative stress of NRVMs was determined by a glutathione/oxidized glutathione assay kit. The concentrations of secreted vascular endothelium growth factor (VEGF), insulin like growth factor­1 (IGF­1) and basic fibroblast growth factor (bFGF) in the culture medium were quantified by enzyme­linked immunosorbent assay. Under both normoxia and physioxia, co­culture with ASCs protected H2O2­exposed NRVMs from apoptosis and significantly alleviated the oxidative stress in NRVMs. The protective effects of ASCs were associated with increased secretion of VEGF, IGF­1 and bFGF. ASCs cultured in 5% O2 exhibited certain cardioprotective effects against H2O2 stress. The results of the present study suggested that O2 concentrations influenced the cardioprotective effects of ASCs. VEGF, IGF­1 and bFGF may serve a role in the myocardial regeneration mediated by transplanted ASCs.


Subject(s)
Adipocytes/metabolism , Adipose Tissue/metabolism , Bodily Secretions/metabolism , Cardiotonic Agents/metabolism , Intercellular Signaling Peptides and Proteins/metabolism , Stem Cells/metabolism , Animals , Apoptosis/physiology , Cell Hypoxia/physiology , Cells, Cultured , Coculture Techniques/methods , Culture Media, Conditioned/metabolism , Hydrogen Peroxide/metabolism , Insulin-Like Growth Factor I/metabolism , Male , Myocytes, Cardiac/metabolism , Oxidative Stress/physiology , Rats , Rats, Sprague-Dawley , Vascular Endothelial Growth Factor A/metabolism
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