| First Author | Noga AA | Year | 2003 |
| Journal | J Biol Chem | Volume | 278 |
| Issue | 8 | Pages | 5952-5 |
| PubMed ID | 12482759 | Mgi Jnum | J:81995 |
| Mgi Id | MGI:2450492 | Doi | 10.1074/jbc.M212194200 |
| Citation | Noga AA, et al. (2003) Plasma homocysteine is regulated by phospholipid methylation. J Biol Chem 278(8):5952-5 |
| abstractText | Mild hyperhomocysteinemia is an independent risk factor for cardiovascular disease. Homocysteine, a non-protein amino acid, is formed from S-adenosylhomocysteine and partially secreted into plasma. A potential source for homocysteine is methylation of the lipid phosphatidylethanolamine to phosphatidylcholine by phosphatidylethanolamine N-methyltransferase in the liver. We show that mice that lack phosphatidylethanolamine N-methyltransferase have plasma levels of homocysteine that are approximately 50% of those in wild-type mice. Hepatocytes isolated from methyltransferase-deficient mice secrete approximately 50% less homocysteine. Rat hepatoma cells transfected with phosphatidylethanolamine N-methyltransferase secrete more homocysteine than wild-type cells. Thus, phosphatidylethanolamine N-methyltransferase is an important source of plasma homocysteine and a potential therapeutic target for hyperhomocysteinemia. |
