1991 Fiscal Year Final Research Report Summary
Roles of signal transmitters in vascular endothelial injury by activated platalets and its prevention
Project/Area Number |
02670387
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Circulatory organs internal medicine
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Research Institution | Tokyo Medical and Dental University |
Principal Investigator |
KISHI Yukio Tokyo Medical and Dental Univ., Dept. Medicine, Assistant, 医学部・第三内科, 助手 (70186211)
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Project Period (FY) |
1990 – 1991
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Keywords | Endothelial Cells / Cell Injury / Platelet / Cyclic Nucleotides / Phosphoinositide / Calcium / Adenine Nucleotides / Prostacyclin |
Research Abstract |
An in vitro study was performed to assess injury to vascular endothelial cells. Human platelets, activated by collagen, enhanced the leakage of radioactivity from cultured bovine aortic endothelial cells preloaded with[^3H]adenine ([^3H]adenine release). An analysis of radioactive materials by thin-layer chromatography revealed decreased intracellular ATP content in the cells treated with activated platelets. The medium contained AMP and adenosine, the latter increasing following the treatment of the cells. The[^3H]cyclic AMP showed time-dependent decrease in the prelabeled cells, exposed to the activated platelets. Moreover, activated platelets induced increase in inositol triphosphate- and cytosolic free calcium ion in the endothelial cells. The initial rapid increase in calcium concentration forming a spike was abolished when the activated platelets were pretreated with apyrase. Pretreatment of the endothelial cells with agents elevating the cyclic AMP levels prevented a [^3H]adenine release, while nifedipine or agents which produce effects that increase cyclic GMP levels had little effects. We conclude that calcium ion plays an important role in vascular endothelial injury by activated platelets and agents elevating cyclic AMP may protect the cells from injury by enhancing calcium sequestration.
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