2012 Fiscal Year Final Research Report
Molecular mechanism for anti-thrombotic action of alcohol drinking related to TRP channels of platelets.
| Project/Area Number |
22590562
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
MARUMO Mikio 兵庫医科大学, 医学部, 講師 (40333950)
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| Co-Investigator(Kenkyū-buntansha) |
WAKABAYASHI Ichiro 兵庫医科大学, 医学部, 教授 (70220829)
TAKEDA Yuji 山形大学, 医学部, 助教 (90302299)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 予防医学 / 血栓症 |
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| Research Abstract |
The mechanism for the inhibitory action of alcohol on platelet aggregation is unknown. In this study, effects of ethanol and methanol on capacitative Ca2+ entry and the subsequent aggregation and diacylglycerol-dependent Ca2+ entry and the subsequent aggregation in platelets were investigated. Both Ca2+ entry pathways are known to be mediated by TRP channels. Aggregation of washed platelets was significantly inhibited by ethanol irrespective of the kind of stimulant for platelets, and similar inhibition was found in platelets in the whole blood by using the modified SFP method. On the other hand, capacitative Ca2+ entry and diacylglycerol-dependent Ca2+ entry were significantly inhibited and augmented, respectively, by ethanol. Therefore, ethanol showed diverse effects on Ca2+ entry through different mechanisms such as intracellular Ca2+-store depletion and stimulation by diacylglycerol. Consequently, thrombin-induced Ca2+ entry, which is thought to be the sum of the above two knds of Ca2+ entry, was not significantly altered by ethanol. Methanol showed no significant effects on capacitative Ca2+ entry and diacylglycerol-dependent Ca2+ entry, while thrombin-induced platelet aggregation was significantly augmented by methanol. Thus, the effects of alcohol on platelet function vary with the kind of alcohol as well as the kind of stimulant.
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