Journal article
Role of Endoplasmic Reticulum Calcium Disequilibria in the Mechanism of Homocysteine-Induced ER Stress
Abstract
Our laboratory demonstrated that hyperhomocysteinemia accelerates atherosclerosis in mouse models through ER stress and activation of the unfolded protein response (UPR). In this study, we tested the hypothesis that homocysteine-induced ER stress may arise from ER-Ca(2+) disequilibria. We found that homocysteine-induced cytosolic Ca(2+) transients in T24/83 cells and human aortic smooth muscle cells (HASMCs). These calcium effects occurred at …
Authors
Dickhout JG; Sood SK; Austin RC
Journal
Antioxidants & Redox Signaling, Vol. 9, No. 11, pp. 1863–1874
Publisher
Mary Ann Liebert
Publication Date
11 2007
DOI
10.1089/ars.2007.1780
ISSN
1523-0864
Associated Experts
Fields of Research (FoR)
Medical Subject Headings (MeSH)
AortaCalcimycinCalciumCell Line, TumorDose-Response Relationship, DrugEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPFluorescent Antibody Technique, IndirectFluorescent DyesFura-2Heat-Shock ProteinsHomocysteineHumansIonophoresMolecular ChaperonesMuscle, Smooth, VascularOxidative StressThapsigarginTime FactorsUrinary Bladder Neoplasms