Can atypical response in endothelial dysfunction-related genes and microRNAs arise from low hydrogen peroxide exposure?

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dc.contributor.authorUrhan-kucuk, Meral
dc.contributor.authorTerzi, Menderes Yusuf
dc.date.accessioned2024-09-18T20:53:03Z
dc.date.available2024-09-18T20:53:03Z
dc.date.issued2024
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractOBJECTIVE: Vascular endothelium is a tissue in which several vasoactive substances are produced and secreted. Reactive oxygen species can cause endothelial dysfunction (ED). miRNAs can be implicated in the oxidative stress-related ED during vascular disease pathogeneses. Our aim is to investigate effect of H2O2- induced oxidative stress on expression levels of genes and miRNAs that are key players in ED. METHODS: H2O2 effect on cell viability of human umbilical-vein endothelial cells (HUVEC) at 24-hour was measured with MTT. Low sub-cytotoxic H2O2 concentrations (25, 50 mu M) were selected to analyze their oxidative stress-inducing capacities with MDA assay and their effects on EDN1, NOS3, VCAM1, SERPINE1, miR21, miR22, miR126, and miR146a levels with RT-qPCR. RESULTS: Each tested H2O2 concentration reduced HUVEC cell viability. Fifty mu M H2O2 augmented cellular MDA levels. Intriguingly, EDN1, VCAM1, and SERPINE1 and all analyzed miRNAs' levels attenuated upon H2O2 treatment whereas there was no change in NOS3 levels compared to control. There was a positive correlation between miR-21 and VCAM1. CONCLUSION: Rat her than individual alterations in analyzed parameters, consistent changes in our findings i.e., parallel decreases in EDN1, VCAM1, SERPINE1 mRNA levels as well as miRNAs, suggests that H2O2 concentration-dependent modulation of expression patterns can bring about various impacts on ED (Tab. 1, Fig. 5, Ref. 63). Tex t in PDF www.elis.sken_US
dc.identifier.doi10.4149/BLL_2024_021
dc.identifier.endpage132en_US
dc.identifier.issn0006-9248
dc.identifier.issn1336-0345
dc.identifier.issue2en_US
dc.identifier.pmid38219067en_US
dc.identifier.scopus2-s2.0-85182295143en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage125en_US
dc.identifier.urihttps://doi.org/10.4149/BLL_2024_021
dc.identifier.urihttps://hdl.handle.net/20.500.12483/11554
dc.identifier.volume125en_US
dc.identifier.wosWOS:001202183600003en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAepress Sroen_US
dc.relation.ispartofBratislava Medical Journal-Bratislavske Lekarske Listyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectoxidative stressen_US
dc.subjectendothelial dysfunctionen_US
dc.subjectmicroRNAen_US
dc.subjectgene expressionen_US
dc.titleCan atypical response in endothelial dysfunction-related genes and microRNAs arise from low hydrogen peroxide exposure?en_US
dc.typeArticleen_US

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