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Prostaglandin synthase 2 gene disruption causes severe renal pathology in the mouse
Open accessAbstract
The prostaglandin endoperoxide H synthase isoform 2, cyclooxygenase 2 (COX-2), is induced at high levels in migratory and other responding cells by pro-inflammatory stimuli. COX-2 is generally considered to be a mediator of inflammation. Its isoform, COX-1, is constitutively expressed in most tissues and is thought to mediate "housekeeping" functions. These two enzymes are therapeutic targets of the widely used nonsteroidal anti-inflammatory drugs (NSAIDs). To investigate further the different physiologic roles of these isoforms, we have used homologous recombination to disrupt the mouse gene encoding COX-2 (Ptgs2). Mice lacking COX-2 have normal inflammatory responses to treatments with tetradecanoyl phorbol acetate or with arachidonic acid. However, they develop severe nephropathy and are susceptible to peritonitis.
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Metadata
- Authors
- Morham, S. G., Langenbach, R., Loftin, C. D., Tiano, H. F., Vouloumanos, N., Jennette, J. C., Mahler, J. F., Kluckman, K. D., Ledford, A., Lee, C. A., & Smithies, O.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1995-11
- Volume
- 83
- Issue
- 3
- Pages
- 473-482
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2083651943
- Cited by
- 1,082
- References
- 2
- FWCI
- 46.63
- Type
- journal article
- Language
- en
- Open access
- bronze
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