Inhibition of endoplasmic reticulum stress protected DOCA-salt hypertension-induced vascular dysfunction

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dc.authorid0000-0002-6422-1203en_US
dc.contributor.authorHan, Sevtap
dc.contributor.authorBal, Nur Banu
dc.contributor.authorSadi, Gökhan
dc.contributor.authorUsanmaz, Suzan Emel
dc.contributor.authorTuğlu, Merve Matilda
dc.contributor.authorUludağ, Mecit Orhan
dc.contributor.authorDemirel-Yılmaz, Emine
dc.date.accessioned2019-12-06T21:15:13Z
dc.date.available2019-12-06T21:15:13Z
dc.date.issued2019
dc.departmentKMÜ, Kamil Özdağ Fen Fakültesi, Biyoloji Bölümüen_US
dc.descriptionWOS:000462806800005en_US
dc.descriptionPubMed:30458302en_US
dc.description.abstractHypertension has complex vascular pathogenesis and therefore the molecular etiology remains poorly elucidated. Endoplasmic reticulum stress (ERS), which is a condition of the unfolded/misfolded protein accumulation in the endoplasmic reticulum, has been defined as a potential target for cardiovascular disease. In the present study, the effects of ERS inhibition on hypertension-induced alterations in the vessels were investigated. In male Wistar albino rats, hypertension was induced through unilateral nephrectomy, deoxycorticosteroneacetate (DOCA) injection (20 mg/kg, twice a week) and 1% NaCl with 0.2% KCI added to drinking water for 12 weeks. An ERS inhibitor, tauroursodeoxycolic acid (TUDCA) (150 mg/kg/day, i.p.), was administered for the final four weeks. ERS inhibition in DOCA-salt induced hypertension was observed to have reduced systolic blood pressure, improved endothelial dysfunction, enhanced plasma nitric oxide (NO) level, reduced protein expressions of phosphorylated-double-stranded RNA-activated protein kinase-like endoplasmic reticulum kinase (pPERK), 78 kDa glucose-regulated protein (GRP78), Inositol trisphosphate receptor1 (IP(3)R1) and Epidermal growth factor receptor (EGFR), increased expressions of endoplasmic reticulum Ca2+-ATPase2 (SERCA2) and B cell lymphoma2 (Bcl2) in vessels. These findings suggest that the beneficial effects of ERS inhibition on hypertension may be related to protection of vessel functions through restoration of endoplasmic reticulum calcium homeostasis, and apoptotic and mitotic pathways.en_US
dc.description.sponsorshipAnkara University Research FoundationAnkara University [16B0230004]en_US
dc.description.sponsorshipThis study was supported by a research grant (16B0230004) from the Ankara University Research Foundation. The authors are grateful to Prof. Dr. H. Gurdal and B. Dalkilic for assisting with the Western Blot analysis.en_US
dc.identifier.citationHan, S., Bal, N. B., Sadi, G., Usanmaz, S. E., Tuğlu, M. M., Uludağ, M. O. (2019). Inhibition of endoplasmic reticulum stress protected DOCA-salt hypertension-induced vascular dysfunction. Vascular Pharmacology, 113, 38-46.
dc.identifier.doi10.1016/j.vph.2018.11.004
dc.identifier.endpage46en_US
dc.identifier.issn1537-1891
dc.identifier.issn1879-3649
dc.identifier.pmid30458302
dc.identifier.scopus2-s2.0-85056854400
dc.identifier.scopusqualityQ2
dc.identifier.startpage38en_US
dc.identifier.urihttps://dx.doi.org/10.1016/j.vph.2018.11.004
dc.identifier.urihttps://hdl.handle.net/11492/2497
dc.identifier.volume113en_US
dc.identifier.wosWOS:000462806800005
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Sceince
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorSadi, Gökhan
dc.language.isoen
dc.publisherElsevier Science Incen_US
dc.relation.journalVascular Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectHypertensionen_US
dc.subjectEndoplasmic Reticulum Stressen_US
dc.subjectVascular Dysfunctionen_US
dc.subjectTUDCAen_US
dc.titleInhibition of endoplasmic reticulum stress protected DOCA-salt hypertension-induced vascular dysfunctionen_US
dc.typeArticle

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