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An early transient decrease in phosphatidylinositol 4,5-bisphosphate upon stimulation of rabbit platelets with acetylglycerylether phosphorylcholine (platelet activating factor).

作者信息

Shukla S D, Hanahan D J

出版信息

Arch Biochem Biophys. 1983 Dec;227(2):626-9. doi: 10.1016/0003-9861(83)90492-7.

DOI:10.1016/0003-9861(83)90492-7
PMID:6320731
Abstract

Washed rabbit platelets labeled with [3H]inositol were stimulated with AGEPC (1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine) (5 X 10(-10) M) for various time periods. Within 5 s of the mixing of these platelets with AGEPC, an approximately 25% decrease in the [3H]TPI (phosphatidylinositol 4,5-bisphosphate) was evident; immediately thereafter the radioactivity in TPI increased. These labeled platelets treated with various concentrations of AGEPC for only 5 s indicated a characteristic dose-related decrease in [3H]TPI. Radioactivity in phosphatidylinositol 4-phosphate also appeared to increase after AGEPC-induced stimulation of platelets. Interestingly, within 15 s a 15 to 20% decrease in [3H]PI (phosphatidylinositol) and an increase in [3H]lysoPI was observed. However, [3H]lysoPI could be related only to one-third of the decrease in [3H]PI. LysoGEPC (lyso-1-O-alkyl-sn-glyceryl-3-phosphorylcholine), which is ineffective in the activation of platelets, was unable to cause any changes in the phosphoinositides. The fact that the status of TPI was influenced in a time- and dose-dependent manner and the rapidity with which these changes take place suggest that this inositol phospholipid may be associated closely with the early processes which accompany the interaction of AGEPC with platelets.

摘要

相似文献

1
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引用本文的文献

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2
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3
Inhibition by the PAF antagonist WEB 2086 of PAF induced inositol-1,4,5-trisphosphate production in human platelets.
Lipids. 1991 Dec;26(12):1050-3. doi: 10.1007/BF02536500.
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Inositol phospholipid turnover in PAF transmembrane signalling.
Lipids. 1991 Dec;26(12):1028-33. doi: 10.1007/BF02536496.