Metabolism of 1-alkyl-2-acyl-GPC in human platelets in response to stimulation by thrombin.
Washed human platelets were incubated with radioactive 1-[3H]alkyl-2-hydroxyglycero-3-phosphocholine (lyso-PAF) at 37 degrees C. [3H]lyso-PAF was converted by platelets into [3H]alkylacyl-GPC which was incorporated. Incorporation of radioactivity was time dependent and reached a maximum of 57 percent in one h. This formation and incorporation of [3H]alkylacyl-GPC was inhibited (50%) by extracellular calcium (1.3 mM). Labeled platelets were treated for 5 min with either thrombin (2.5 U/ml) or saline solution. While there was no change in the saline control, thrombin induced a reduction in the content of [3H]alkylacyl-GPC, accompanied by an increase in [3H]lyso-PAF presumably by stimulation of phospholipase A2. There was no apparent increase in radioactivity comigrating with PAF. This was probably due to the overwhelming dilution of the radioactive alkylacyl-GPC by the endogenous nonradioactive compound (ratio-1/3200). These studies suggest that human platelets can take up lyso-PAF and acylate it to alkylacyl-GPC which is susceptible to phospholipase A2 activity.
D000215:Acylation; D000328:Adult; D000818:Animals; D001792:Blood Platelets / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D006801:Humans; D010741:Phospholipases A / Q000502:physiology; D054467:Phospholipases A2; D010972:Platelet Activating Factor / Q000031:analogs & derivatives* / Q000096:biosynthesis / Q000097:blood; D010974:Platelet Aggregation / Q000187:drug effects; D011817:Rabbits; D013917:Thrombin / Q000494:pharmacology*; D014316:Tritium
C036761:1-alkyl-2-acyl-sn-glycero-3-phosphocholine; D010972:Platelet Activating Factor; D014316:Tritium; D010741:Phospholipases A; D054467:Phospholipases A2; D013917:Thrombin