Abstract:
:Prostaglandins have wide-ranging effects in the body and are thought to be important mediators of inflammation. Cyclooxygenase (COX) plays a key regulatory role in prostaglandin synthesis, and occurs in both constitutive (COX-1) and inducible (COX-2) isoforms. COX-1 is thought to provide cytoprotective effects, whereas COX-2 is both inducible and the major isoform of inflammatory cells. Reduction of prostaglandin production by inhibition of cyclooxygenases appears to be the main mechanism of action of most non-steroidal anti-inflammatory drugs (NSAIDS). Here we present an animal model of COX-2 deficiency that was generated by gene targeting. Defects in null mice correlating with reduced viability included renal alterations, characteristic of renal dysplasia (100% penetrance), and cardiac fibrosis (50% penetrance). Female Cox-2-/- mice were infertile. COX-2 deficiency failed to alter inflammatory responses in several standard models, but striking mitigation of endotoxin-induced hepatocellular cytotoxicity was observed.
journal_name
Naturejournal_title
Natureauthors
Dinchuk JE,Car BD,Focht RJ,Johnston JJ,Jaffee BD,Covington MB,Contel NR,Eng VM,Collins RJ,Czerniak PMdoi
10.1038/378406a0subject
Has Abstract,Author List Incompletepub_date
1995-11-23 00:00:00pages
406-9issue
6555eissn
0028-0836issn
1476-4687journal_volume
378pub_type
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