Human platelet phospholipid methylation |
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| Authors: | Donna Mandio Cordasco David J Segarnick John Rotrosen |
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| Institution: | 1. Psychiatry Service New York Veterans Administration Medical Center New York, New York 10010, USA;2. Department of Psychiatry New York University School of Medicine 550 First Avenue New York, New York 10016, USA |
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| Abstract: | Intact platelets actively incorporate 3H-methionine and successively methylate phosphatidylethanolamine to 3H-phosphatidyl- N-monomethylethanolamine (PME), 3H-phosphatidyl-N, N-dimethylethanolamine (PDE) and 3H-phosphatidylcholine (PC) in platelet membranes. Phospholipid methylation is dependent on time, temperature, pH and methionine concentration. Thrombin, epinephrine and adenine potently inhibit phospholipid methylation and to a lesser degree enhance degradation of 3H-methylated phospholipids. Unlike 3H-methylated phospholipids in red cells and synaptosomes, 3H-PME, 3H-PDE and 3H-PC are symmetrically distributed on both sides of platelet membranes. Furthermore, in contrast to leukocytes, methylation derived PC is not distinguishable from CDP-choline derived PC as a substrate for arachidonic acid release since platelets labelled with 3H-methionine, 3H-choline and 14C-arachidonic acid all showed similar degradation of labelled PC when stimulated with thrombin. 3H-S-adenosyl-L-methionine (SAM) is not actively incorporated by intact platelets; however, lysed platelet membrane fragments were able to utilize 3H-SAM as a methyl donor. Addition of exogenous phospholipids enhanced product formation. |
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| Keywords: | to whom correspondence should be addressed |
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