| G2A plays proinflammatory roles in human keratinocytes under oxidative stress as a receptor for 9-hydroxyoctadecadienoic acid. | |
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MedLine Citation:
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PMID: 18034171 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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G2A is a stress-inducible G protein-coupled receptor for oxidized free fatty acids, such as 9-hydroxyoctadecadienoic acid (HODE). As skin is routinely and pathologically exposed to many oxidative stresses such as UV radiation, chemical agents, and inflammation that might induce both G2A expression and production of G2A ligands, we examined G2A function in human keratinocytes. G2A was expressed in human epidermis, normal human epidermal keratinocytes (NHEK), and an immortalized human keratinocyte cell line (HaCaT). 9(S)-HODE evoked intracellular calcium mobilization and secretion of cytokines, including IL-6, IL-8, and GM-CSF in NHEK cells. These responses became prominent in HaCaT cells by overexpression of G2A. 9(S)-HODE inhibited proliferation of NHEK cells by suppressing DNA synthesis and arresting the cell cycle in the G0/1-phase. On the other hand, 13(S)-HODE, another major oxidative product from linoleate, showed little or no effect on either cytokine secretion or on proliferation in NHEK cells. A small interfering RNA designed to downregulate G2A caused suppression of 9(S)-HODE-induced inhibitory effects on proliferation of NHEK cells. UVB and H(2)O(2) induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. These results suggest that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions. |
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Authors:
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Tomoyasu Hattori; Hideru Obinata; Ai Ogawa; Mikiko Kishi; Kazuaki Tatei; Osamu Ishikawa; Takashi Izumi |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-11-22 |
Journal Detail:
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Title: The Journal of investigative dermatology Volume: 128 ISSN: 1523-1747 ISO Abbreviation: J. Invest. Dermatol. Publication Date: 2008 May |
Date Detail:
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Created Date: 2008-04-14 Completed Date: 2008-05-19 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0426720 Medline TA: J Invest Dermatol Country: United States |
Other Details:
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Languages: eng Pagination: 1123-33 Citation Subset: IM |
Affiliation:
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Department of Molecular Biochemistry, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Calcium
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metabolism Cell Cycle Proteins / genetics, metabolism* Cell Division / drug effects, physiology Cells, Cultured Cytokines / metabolism, secretion Dermatitis / metabolism* Epidermis / cytology G0 Phase / drug effects, physiology G1 Phase / drug effects, physiology Gene Expression / drug effects, immunology, radiation effects Humans Hydrogen Peroxide / pharmacology Keratinocytes / cytology, immunology*, metabolism Linoleic Acids, Conjugated / metabolism*, pharmacology Oxidants / pharmacology Oxidative Stress / immunology* RNA, Messenger / metabolism Receptors, G-Protein-Coupled / genetics, metabolism* Signal Transduction / drug effects, immunology Ultraviolet Rays |
| Chemical | |
Reg. No./Substance:
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0/Cell Cycle Proteins; 0/Cytokines; 0/G2A receptor; 0/Linoleic Acids, Conjugated; 0/Oxidants; 0/RNA, Messenger; 0/Receptors, G-Protein-Coupled; 15514-85-9/9-hydroxy-10,12-octadecadienoic acid; 7440-70-2/Calcium; 7722-84-1/Hydrogen Peroxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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