Renal abnormalities and an altered inflammatory response in mice lacking cyclooxygenase II View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1995-11

AUTHORS

Joseph E. Dinchuk, Bruce D. Car, Richard J. Focht, Jennifer J. Johnston, Bruce D. Jaffee, Maryanne B. Covington, Nancy R. Contel, Vicki M. Eng, Robert J. Collins, Philip M. Czerniak, Stewart A. Gorry, James M. Trzaskos

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. More... »

PAGES

406-409

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/378406a0

DOI

http://dx.doi.org/10.1038/378406a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1028548438

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/7477380


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