{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Aguado A"],"funding":["British Heart Foundation","NCI NIH HHS","Canadian Institutes of Health Research"],"pagination":["253-65"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4947528"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["34(2)"],"pubmed_abstract":["<h4>Objective</h4>NOX-1 and NOX-4 are key enzymes responsible for reactive oxygen species (ROS) generation in vascular smooth muscle cells (VSMC). The RNA-binding protein Hu antigen R (HuR) is implicated in posttranscriptional regulation of gene expression; however, its role regulating NOX is unknown. We investigated transcriptional and posttranscriptional mechanisms underlying angiotensin II (AngII) and IL-1β regulation of NOX-1 and NOX-4 in VSMC and their implications in cell migration.<h4>Methods</h4>Rat and human VSMC were stimulated with AngII (0.1 μmol/l) and/or IL-1β (10 ng/ml). NOX-1 and NOX-4 mRNA and protein levels, NOX-1 and NOX-4 promoter and 3'UTR activities, NADPH oxidase activity, ROS production, and cell migration were studied.<h4>Results</h4>IL-1β increased NOX-1 expressio"],"journal":["Journal of hypertension"],"pubmed_title":["Hu antigen R is required for NOX-1 but not NOX-4 regulation by inflammatory stimuli in vascular smooth muscle cells."],"pmcid":["PMC4947528"],"funding_grant_id":["R01 CA134609","R01CA134609","RG/13/7/30099"],"pubmed_authors":["Salaices M","Fischer T","Martinez-Gonzalez J","Manea A","Aguado A","Briones AM","Rodriguez C","Alonso MJ","Dixon DA","Hernanz R","Touyz RM"],"additional_accession":[]},"is_claimable":false,"name":"Hu antigen R is required for NOX-1 but not NOX-4 regulation by inflammatory stimuli in vascular smooth muscle cells.","description":"<h4>Objective</h4>NOX-1 and NOX-4 are key enzymes responsible for reactive oxygen species (ROS) generation in vascular smooth muscle cells (VSMC). The RNA-binding protein Hu antigen R (HuR) is implicated in posttranscriptional regulation of gene expression; however, its role regulating NOX is unknown. We investigated transcriptional and posttranscriptional mechanisms underlying angiotensin II (AngII) and IL-1β regulation of NOX-1 and NOX-4 in VSMC and their implications in cell migration.<h4>Methods</h4>Rat and human VSMC were stimulated with AngII (0.1 μmol/l) and/or IL-1β (10 ng/ml). NOX-1 and NOX-4 mRNA and protein levels, NOX-1 and NOX-4 promoter and 3'UTR activities, NADPH oxidase activity, ROS production, and cell migration were studied.<h4>Results</h4>IL-1β increased NOX-1 expressio","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Feb","modification":"2025-04-03T23:47:42.708Z","creation":"2019-03-27T02:18:32Z"},"accession":"S-EPMC4947528","cross_references":{"pubmed":["26682942"],"doi":["10.1097/hjh.0000000000000801","10.1097/HJH.0000000000000801"]}}