2001 Fiscal Year Final Research Report Summary
Molecular biological study on pithophysiology of chronic muscle pain from the view of abnormal beta2-adrenergic receptor function.
Project/Area Number |
12671883
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
補綴理工系歯学
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Research Institution | OKAYAMA UNIVERSITY |
Principal Investigator |
MAEKAWA Kenji Okayama University, Dental Hospital, Assistant Professor, 歯学部・附属病院, 講師 (20304313)
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Co-Investigator(Kenkyū-buntansha) |
MINAKUCHI Hajime Okayama University, Graduate School of Med and Dent, Research Associate, 大学院・医歯学総合研究科, 助手 (30325097)
SUZUKI Kouji Okayama University, Graduate School of Med and Dent, Research Associate, 大学院・医歯学総合研究科, 助手 (30304322)
KUBOKI Takuo Okayama University, Graduate School of Med and Dent, Associate Professor, 大学院・医歯学総合研究科, 助教授 (00225195)
YATANI Hirofumi Okayama University, Graduate School of Med and Dent, Professor, 大学院・医歯学総合研究科, 教授 (80174530)
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Project Period (FY) |
2000 – 2001
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Keywords | chronic muscle pain / beta2 adrenergic receptor / cAMP / fibromyalgia / localized myalgia |
Research Abstract |
The purpose of this study was to investigate alteration of the beta-adrenergic receptor (BAR) in fibromyalgia and chronic localized myalgia patients. Since the BARs are present on circulating lymphocytes and activation of the G-protein coupled receptors like BAR leads to an increase in the intracellular level of cyclic adenosine monophosphate (cAMP), we measured cAMP levels to assess indirectly the functional status of the receptor. Thirty cc peripheral blood samples were drawn from subjects' anterocubital vein. Lymphocyte cells were isolated from the total blood by using the Ficoll-Hypaque gradient technique. Basal and stimulated intracellular cAMP levels were determined by enzyme immunoassay using a commercially available kit (cAMP EIA system, Amersham, England). Aliquots of even amount of cells were incubated with or without stimulation of beta-agonist isoproterenol (ISO) for 5min. Results : Basal intracellular cAMP levels were not significantly different between FM patients and healthy controls and between localized myalgia and healthy controls. However, beta-agonist induced mean intracellular cAMP increase was significantly reduced in FM patients compared with controls. Regarding the localized myalgia patients, beta-agonist induced mean intracellular cAMP increase was almost identical with that of controls (p=0.806). These results suggest that diminished βAR function might be related to FM pathophysiology. In addition, these findings indirectly support the notion that the pathophysiology of fibromyalgia and localized myalgia are different.
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Research Products
(12 results)