{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T19:11:43Z","timestamp":1790709103315,"version":"4.1.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[1996,3,1]]},"abstract":"<jats:p> Prostaglandin endoperoxide synthase-1 [prostaglandin G\/H synthase-1 (PGHS-1)] and PGHS-2 are key enzymes in the conversion of arachidonic acid to prostaglandins and other eicosanoids. We refer to these isoforms as cyclooxygenase-1 (COX-1) and COX-2 in this review. This brief review focuses on recent developments in the study of these enzymes. Alterations in the expression levels of COX-2 result in distinct phenotypic changes in intestinal epithelial cells. Overexpression of COX-2 in intestinal epithelial cells results in increased adhesion to extracellular matrix proteins and inhibition of apoptosis. Disruption of the COX-2 gene in mice results in renal dysplasia, cardiac fibrosis, and defects in the ovary. Interestingly, disruption of the COX-1 gene results in distinct phenotypic changes different from those observed for COX-2. COX-1 null mice survive well, have no gastric pathology, and show less indomethacin-induced gastric ulceration than wild-type mice. These two closely related enzymes must have distinct functions in the organisms, since lack of their expression causes distinct phenotypic changes for each respective isoform. <\/jats:p>","DOI":"10.1152\/ajpgi.1996.270.3.g393","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T10:54:07Z","timestamp":1514112847000},"page":"G393-G400","source":"Crossref","is-referenced-by-count":57,"title":["Prostaglandin endoperoxide synthase: why two isoforms?"],"prefix":"10.1152","volume":"270","author":[{"given":"C. S.","family":"Williams","sequence":"first","affiliation":[{"name":"Department of Medicine, Vanderbilt University Medical Center,Nashville, Tennessee 37232-2279, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. N.","family":"DuBois","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University Medical Center,Nashville, Tennessee 37232-2279, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajpgi.1996.270.3.G393","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:12:29Z","timestamp":1567987949000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajpgi.1996.270.3.G393"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,3,1]]}},"alternative-id":["10.1152\/ajpgi.1996.270.3.G393"],"URL":"https:\/\/doi.org\/10.1152\/ajpgi.1996.270.3.g393","relation":{},"ISSN":["0193-1857","1522-1547"],"issn-type":[{"value":"0193-1857","type":"print"},{"value":"1522-1547","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,3,1]]}}}