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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:679.)
© 2005 American Heart Association, Inc.

Brief Reviews

Transcriptional Control of COX-2 via C/EBPß

Kenneth K. Wu; Jun-Yang Liou; Katarzyna Cieslik

From the Vascular Biology Research Center, Institute of Molecular Medicine and Division of Hematology, University of Texas Health Science Center at Houston, Tex.

Correspondence to Kenneth K. Wu, Vascular Biology Research Center, Institute of Molecular Medicine and Division of Hematology, University of Texas Health Science Center at Houston, 6431 Fannin, MSB 5.016, Houston, TX 77030. E-mail Kenneth.K.Wu{at}uth.tmc.edu

Cyclooxygenase-2 (COX-2) is a highly inducible enzyme exerting diverse actions on cell functions, including proliferation, migration, and DNA damage. Enhanced COX-2 expression may be protective, but excessive expression may be harmful, causing inflammation, atheromatous plaque instability, and intimal hyperplasia. COX-2 transcriptional activation by proinflammatory mediators has been extensively characterized. In this review, the role of C/EBP in regulating COX-2 transcription is highlighted. Recent advances in control of COX-2 transcription by aspirin and salicylate and by a cell cycle-dependent endogenous mechanism are described. The recent progress sheds light on the pathophysiological mechanisms of COX-2 and new transcription-based strategy for controlling COX-2 overexpression and COX-2–mediated cardiovascular diseases.

Cyclooxygenase-2 (COX-2) is a highly inducible enzyme exerting diverse actions on cell functions, including proliferation, migration, and DNA damage. Enhanced COX-2 expression may be protective, but excessive expression may be harmful, causing inflammation, atheromatous plaque instability, and intimal hyperplasia. In this review, the role of C/EBP in regulating COX-2 transcription is highlighted.

Key Words: aspirin • C/EBP • COX-2 • inflammation • NF-B

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