Tumor necrosis factor-α promotes sustained cyclooxygenase-2 expression: Attenuation by dexamethasone and NSAIDs

Prostaglandins

Volumn 54, Issue 4, 1997, Pages 727-743

  Perkins, Douglas J ^a   Kniss, Douglas A ^a,b  

^a OHIO STATE UNIVERSITY   (United States)

^b THE OHIO STATE UNIVERSITY COLLEGE OF MEDICINE   (United States)

Author keywords

Cyclooxygenase 2; Dexamethasone; NSAID; Tumor necrosis factor

Indexed keywords

ARACHIDONIC ACID; CYCLOOXYGENASE 2; DEXAMETHASONE; INDOMETACIN; MESSENGER RNA; N (2 CYCLOHEXYLOXY 4 NITROPHENYL)METHANESULFONAMIDE; NONSTEROID ANTIINFLAMMATORY AGENT; PROSTAGLANDIN E2; RECOMBINANT TUMOR NECROSIS FACTOR ALPHA;

AMNION CELL; AMNION FLUID; ARACHIDONIC ACID METABOLISM; ARTICLE; CONTROLLED STUDY; DECIDUA; ENZYME ACTIVITY; ENZYME INDUCTION; HUMAN; HUMAN CELL; INFLAMMATION; MESSENGER RNA SYNTHESIS; PROSTAGLANDIN SYNTHESIS; PROTEIN EXPRESSION;

AMNION; ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL; CELLS, CULTURED; CYCLOOXYGENASE 1; CYCLOOXYGENASE 2; DEXAMETHASONE; DINOPROSTONE; DOSE-RESPONSE RELATIONSHIP, DRUG; GLUCOCORTICOIDS; HUMANS; ISOENZYMES; MEMBRANE PROTEINS; PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES; RNA, MESSENGER; TUMOR NECROSIS FACTOR-ALPHA;

EID: 0031434540     PISSN: 00906980     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0090-6980(97)00144-5     Document Type: Article

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