Abstract
A variety of factors contribute to the complex course of inflammation. Microbiological, immunological and toxic agents can initiate the inflammatory response by activating a variety of humoral and cellular mediators. In the early phase of inflammation, excessive amounts of cytokines and inflammatory mediators are released. These factors activate, in addition to other signaling pathways, the lipid synthesis pathways, which play a crucial role in the pathogenesis of organ dysfunction. Arachidonic acid (AA), the precursor of pro-inflammatory eicosanoids, is released from membrane phospholipids by the action of phospholipase A2 (PLA2), and is metabolized to prostaglandins (PGs) and leukotrienes (LTs) by the action of cyclooxygenase (COX) and lipoxygenase (LO) enzymes, respectively. Disordered activation of PLA2, LO and COX enzymes have been implicated in many inflammatory diseases. PLA2 is activated by phospholipase-A2-activating protein (PLAP) and LO by 5-lipoxygenase-activating protein (FLAP). The inducible form of COX-2 enzyme, which is usually not present under basal conditions, is induced in inflammation. In this article the function of these enzymes in eicosanoid synthesis, their regulation, and their implication in inflammatory disorders will be reviewed. The properties, function and regulation of the protein activators PLAP and FLAP will also be discussed.
Keywords: Eicosanoid Synthesis, toxic agents, cyclooxygenase, 5-lipoxygenase-activating protein
Current Protein & Peptide Science
Title: Protein Regulators of Eicosanoid Synthesis: Role in Inflammation
Volume: 3 Issue: 4
Author(s): Fadia R. Homaidan, Iman Chakroun, Hounaida Abi Haidar and Marwan E. El-Sabban
Affiliation:
Keywords: Eicosanoid Synthesis, toxic agents, cyclooxygenase, 5-lipoxygenase-activating protein
Abstract: A variety of factors contribute to the complex course of inflammation. Microbiological, immunological and toxic agents can initiate the inflammatory response by activating a variety of humoral and cellular mediators. In the early phase of inflammation, excessive amounts of cytokines and inflammatory mediators are released. These factors activate, in addition to other signaling pathways, the lipid synthesis pathways, which play a crucial role in the pathogenesis of organ dysfunction. Arachidonic acid (AA), the precursor of pro-inflammatory eicosanoids, is released from membrane phospholipids by the action of phospholipase A2 (PLA2), and is metabolized to prostaglandins (PGs) and leukotrienes (LTs) by the action of cyclooxygenase (COX) and lipoxygenase (LO) enzymes, respectively. Disordered activation of PLA2, LO and COX enzymes have been implicated in many inflammatory diseases. PLA2 is activated by phospholipase-A2-activating protein (PLAP) and LO by 5-lipoxygenase-activating protein (FLAP). The inducible form of COX-2 enzyme, which is usually not present under basal conditions, is induced in inflammation. In this article the function of these enzymes in eicosanoid synthesis, their regulation, and their implication in inflammatory disorders will be reviewed. The properties, function and regulation of the protein activators PLAP and FLAP will also be discussed.
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Cite this article as:
Homaidan R. Fadia, Chakroun Iman, Haidar Abi Hounaida and El-Sabban E. Marwan, Protein Regulators of Eicosanoid Synthesis: Role in Inflammation, Current Protein & Peptide Science 2002; 3 (4) . https://dx.doi.org/10.2174/1389203023380585
DOI https://dx.doi.org/10.2174/1389203023380585 |
Print ISSN 1389-2037 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5550 |
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