Transcriptional control of COX-2 via C/EBPβ

Kenneth K. Wu; Jun Yang Liou; Katarzyna Cieslik

doi:10.1161/01.ATV.0000157899.35660.61

Transcriptional control of COX-2 via C/EBPβ

Kenneth K. Wu, Jun Yang Liou, Katarzyna Cieslik

Houston Methodist

Research output: Contribution to journal › Short survey › peer-review

63 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	679-685
Number of pages	7
Journal	Arteriosclerosis, Thrombosis, and Vascular Biology
Volume	25
Issue number	4
DOIs	https://doi.org/10.1161/01.ATV.0000157899.35660.61
State	Published - Apr 2005

Keywords

Aspirin
C/EBP
COX-2
Inflammation
NF-κB

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1161/01.ATV.0000157899.35660.61

Cite this

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title = "Transcriptional control of COX-2 via C/EBPβ",

abstract = "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.",

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T1 - Transcriptional control of COX-2 via C/EBPβ

AU - Wu, Kenneth K.

AU - Liou, Jun Yang

AU - Cieslik, Katarzyna

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N2 - 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.

AB - 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.

KW - Aspirin

KW - C/EBP

KW - COX-2

KW - Inflammation

KW - NF-κB

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Transcriptional control of COX-2 via C/EBPβ

Abstract

Keywords

ASJC Scopus subject areas

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