S-Space Graduate School of Convergence Science and Technology (융합과학기술대학원) Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과) Journal Papers (저널논문_분자의학 및 바이오제약학과)
15-Deoxy-Δ12,14-prostaglandin J2 as a potential endogenous regulator of redox-sensitive transcription factors
- Kim, Eun-Hee; Surh, Young-Joon
- Issue Date
- Biochemical Pharmacology, Vol.72 No.11, pp.1516-1528
- 15-deoxy-Delta(12,14)-prostaglandin; redox regulation; thiol modification; transcription factors; PPAR-gamma; NF-kappa B; AP-1; Nrf2
- 15-Deoxy-Delta(12,14)-prostaglandin J(2)(15d-PGJ(2)) has been known to display multifaceted cellular functions, including anti-inflammatory and cytoprotective effects. However, depending on the concentrations and intracellular microenvironment, this cyclopentenone prostaglandin can exert opposite effects. Because of the alpha,beta-unsaturated carbonyl moiety present in its cyclopentenone ring structure, 15d-PGJ(2) can act as a Michael reaction acceptor and readily interacts with critical cellular nucleophiles, such as cysteine thiol groups in proteins. Many of the biological effects induced by 15d-PGJ(2) involve redox-transcription factors as the potential targets. Thus, 15d-PGJ(2) can modulate the transcriptional activities of nuclear factor-kappa B (NF-kappa B), activator protein-1 (AP-1), nuclear factor-erythroid 2p45 (NF-E2)-related factors (Nrf2), hypoxia inducible factor (HIF), etc. 15d-PGJ(2) is also well known as an endogenous ligand of peroxisome proliferator-activated receptor gamma (PPAR gamma). However, the regulation of the aforementioned redox-sensitive transcription factors by 15d-PGJ(2) is not necessarily mediated via PPAR gamma activation, but rather involves covalent modification or oxidation of their critical cysteine residues acting as a redox-sensor. This commentary describes the biological and physiological functions of 15d-PGJ(2) and underlying biochemical and molecular mechanisms with emphasis on the modulation of redox-sensitive transcription factors and their regulators. (c) 2006 Elsevier Inc. All rights reserved.
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