| gamma-Aminobutyric acid (A) receptor agonists accelerate cutaneous barrier recovery and prevent epidermal hyperplasia induced by barrier disruption. | |
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MedLine Citation:
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PMID: 12445190 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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gamma-Aminobutyric acid, is an amino acid transmitter, which mediates rapid inhibition in the central nervous system. gamma-Aminobutyric acid (A) receptor is a ligand-gated chloride ion channel playing an important part in polarizing the cell membrane and reducing neuronal excitability in the neuron. In this study, we demonstrated the effects of gamma-aminobutyric acid (A) receptor agonists on the cutaneous barrier repair process after the barrier disruption of hairless mice. Topical application of gamma-aminobutyric acid and gamma-aminobutyric acid (A) receptor-specific agonists, musimol and isoguvacine, after barrier disruption accelerated the barrier recovery. The gamma-aminobutyric acid (B)-specific agonist, baclofen, did not affect the barrier recovery rate. The effect of gamma-aminobutyric acid on the barrier recovery was blocked by the gamma-aminobutyric acid (A)-receptor antagonist, bicuculline methobromide, but gamma-aminobutyric acid (B) receptor antagonist, saclofen, did not affect the effect of gamma-aminobutyric acid. Topical application of gamma-aminobutyric acid also prevented epidermal hyperplasia, which was induced by the barrier insults under low environmental humidity and bicuculline methobromide blocked the effect of gamma-aminobutyric acid on the epidermal hyperplasia. Immunoreactivity against gamma-aminobutyric acid (A) polyclonal antibody was observed in hairless mouse epidermis. The fluorescent probe of gamma-aminobutyric acid (A) receptor, TXR-musimol showed the localization of gamma-aminobutyric acid (A) receptor in the epidermis of the hairless mice. Elevation of intracellular chloride ion was induced by gamma-aminobutyric acid in cultured human keratinocytes and it was blocked by bicuculline methobromide. These results suggest that the gamma-aminobutyric acid (A)-like receptor is associated with skin barrier homeostasis and regulation of the receptor clinically effective for barrier dysfunctional or epidermal hyperproliferative diseases. |
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Authors:
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Mitsuhiro Denda; Kaori Inoue; Shinji Inomata; Sumiko Denda |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The Journal of investigative dermatology Volume: 119 ISSN: 0022-202X ISO Abbreviation: J. Invest. Dermatol. Publication Date: 2002 Nov |
Date Detail:
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Created Date: 2002-11-26 Completed Date: 2003-01-08 Revised Date: 2008-11-21 |
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: 1041-7 Citation Subset: IM |
Affiliation:
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Shiseido Research Center, Fukuura, Kanazawa-ku, Yokohama, Japan. mitsuhiro.denda@to.shiseido.co.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Baclofen / pharmacology Epidermis / metabolism*, pathology GABA Agonists / pharmacology* Humidity Hyperplasia / prevention & control Isonicotinic Acids / pharmacology Male Mice Mice, Hairless Muscimol / pharmacology* Receptors, GABA-A / agonists*, metabolism Wound Healing / drug effects*, physiology |
| Chemical | |
Reg. No./Substance:
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0/GABA Agonists; 0/Isonicotinic Acids; 0/Receptors, GABA-A; 1134-47-0/Baclofen; 2763-96-4/Muscimol; 64603-90-3/isoguvacine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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