{"doi":"10.1152/physiolgenomics.00136.2007","title":"Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension","abstract":"<jats:p> The present study was designed to assess whether or not changes in genomic expression of cyclooxygenases (COX-1, COX-2), endothelial nitric oxide synthase (eNOS), and prostanoid synthases in the endothelium and of prostanoid receptors in vascular smooth muscle contribute to the occurrence of endothelium-dependent contractions during aging and hypertension. Gene expression was quantified by real-time PCR using isolated endothelial cells and smooth muscle cells (SMC) from the aorta of Wistar-Kyoto and spontaneously hypertensive rats. Genes for all known prostanoid synthases and receptors were present in endothelial cells and SMC, respectively. Aging caused overexpression of eNOS, COX-1, COX-2, thromboxane synthase, hematopoietic-type prostaglandin D synthase, membrane prostaglandin E synthase-2, and prostaglandin F synthase in endothelial cells and COX-1 and prostaglandin E<jats:sub>2</jats:sub> (EP)<jats:sub>4</jats:sub> receptors in SMC. Hypertension augmented the expression of COX-1, prostacyclin synthase, thromboxane synthase, and hematopoietic-type prostaglandin D synthase in endothelial cells and prostaglandin D<jats:sub>2</jats:sub> (DP), EP<jats:sub>3</jats:sub>, and EP<jats:sub>4</jats:sub> receptors in SMC. The increase in genomic expression of endothelial COX-1 explains why in aging and hypertension the endothelium has greater propensity to release cyclooxygenase-derived vasoconstrictive prostanoids. The expression of prostacyclin synthase was by far the most abundant, explaining why the majority of the COX-1-derived endoperoxides are transformed into prostacyclin, substantiating the role of prostacyclin as an endothelium-derived contracting factor. The expression of thromboxane synthase was increased in the cells of aging or hypertensive rats, explaining why the prostanoid can contribute to endothelium-dependent contractions. It is uncertain whether the gene modifications caused by aging and hypertension directly contribute to endothelium-dependent contractions or rather to vascular aging and the vascular complications of the hypertensive process. </jats:p>","journal":"Physiological Genomics","year":2008,"id":29633,"datarank":5.586321575388451,"base_score":5.181783550292085,"endowment":5.181783550292085,"self_citation_contribution":0.7772675325438129,"citation_network_contribution":4.809054042844639,"self_endowment_contribution":0.7772675325438129,"citer_contribution":4.809054042844639,"corpus_percentile":null,"corpus_rank":null,"citation_count":177,"citer_count":155,"citers_with_citation_signal":124,"citers_with_endowment":124,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":162968,"name":"Paul M. Vanhoutte","orcid":null,"position":1,"is_corresponding":false},{"id":162966,"name":"Eva H. C. Tang","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"base_score":5.181783550292085,"endowment":5.181783550292085,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"18056786","pmcid":null,"openalex_id":"https://openalex.org/W2153409761","authors":[],"funders":[],"total_grants":0,"fwci":11.2037,"citation_percentile":0.9879171,"influential_citations":13,"citation_trend":[{"year":2012,"count":11},{"year":2013,"count":11},{"year":2014,"count":6},{"year":2015,"count":11},{"year":2016,"count":10},{"year":2017,"count":17},{"year":2018,"count":4},{"year":2019,"count":8},{"year":2020,"count":11},{"year":2021,"count":8},{"year":2022,"count":8},{"year":2023,"count":4},{"year":2024,"count":3},{"year":2025,"count":3},{"year":2026,"count":1}],"oa_status":"closed","license":null,"oa_locations":[{"url":"https://www.physiology.org/doi/pdf/10.1152/physiolgenomics.00136.2007","host_type":"publisher"},{"url":"https://doi.org/10.1152/physiolgenomics.00136.2007","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18056786","host_type":"repository"},{"url":"http://hdl.handle.net/10722/91747","host_type":"repository"}],"fields_of_study":["Inflammatory mediators and NSAID effects","Nitric Oxide and Endothelin Effects","Eicosanoids and Hypertension Pharmacology","Biology","Medicine","Acetylcholine","Aging","Animals","Aorta, Thoracic","Cyclooxygenase 1","Endothelial Cells","Enzyme Induction","Gene Expression Profiling","Gene Expression Regulation","Hypertension","Membrane Proteins","Muscle Proteins","Muscle, Smooth, Vascular","Myocytes, Smooth Muscle","Nitric Oxide Synthase Type II","Nitric Oxide Synthase Type III","Phenylephrine","Prostaglandin-Endoperoxide Synthases","Prostaglandins","Rats","Rats, Inbred SHR","Rats, Inbred WKY","Receptors, Prostaglandin"],"mesh_terms":["Acetylcholine","Aging","Animals","Aorta, Thoracic","Enzyme Induction","Gene Expression Regulation","Hypertension","Membrane Proteins","Muscle Proteins","Muscle, Smooth, Vascular","Phenylephrine","Prostaglandin-Endoperoxide Synthases","Prostaglandins","Rats, Inbred SHR","Rats, Inbred WKY","Receptors, Prostaglandin","Gene Expression Profiling","Myocytes, Smooth Muscle","Endothelial Cells","Rats","Cyclooxygenase 1","Nitric Oxide Synthase Type II","Nitric Oxide Synthase Type III"],"keywords":["Prostacyclin","Prostanoid","Prostaglandin H2","Internal medicine","Endocrinology","Biology","Endothelium","Prostaglandin","Thromboxane-A synthase","Enos","Thromboxane receptor","Thromboxane","Receptor","Vascular smooth muscle","Nitric oxide synthase","Thromboxane A2","Medicine","Platelet","Nitric oxide"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-06-09T00:20:53.418574Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}