| First Author | Rahman SMK | Year | 2022 |
| Journal | Biochim Biophys Acta Mol Cell Biol Lipids | Volume | 1867 |
| Issue | 12 | Pages | 159222 |
| PubMed ID | 35988872 | Mgi Jnum | J:328046 |
| Mgi Id | MGI:7334527 | Doi | 10.1016/j.bbalip.2022.159222 |
| Citation | Rahman SMK, et al. (2022) Formation of N-acyl-phosphatidylethanolamines by cytosolic phospholipase A2epsilon in an ex vivo murine model of brain ischemia. Biochim Biophys Acta Mol Cell Biol Lipids 1867(12):159222 |
| abstractText | N-Acyl-phosphatidylethanolamines (NAPEs), a minor class of membrane glycerophospholipids, accumulate along with their bioactive metabolites, N-acylethanolamines (NAEs) during ischemia. NAPEs can be formed through N-acylation of phosphatidylethanolamine by cytosolic phospholipase A2epsilon (cPLA2epsilon, also known as PLA2G4E) or members of the phospholipase A and acyltransferase (PLAAT) family. However, the enzyme responsible for the NAPE production in brain ischemia has not yet been clarified. Here, we investigated a possible role of cPLA2epsilon using cPLA2epsilon-deficient (Pla2g4e(-/-)) mice. As analyzed with brain homogenates of wild-type mice, the age dependency of Ca(2+)-dependent NAPE-forming activity showed a bell-shape pattern being the highest at the first week of postnatal life, and the activity was completely abolished in Pla2g4e(-/-) mice. However, liquid chromatography-tandem mass spectrometry revealed that the NAPE levels of normal brain were similar between wild-type and Pla2g4e(-/-) mice. In contrast, post-mortal accumulations of NAPEs and most species of NAEs were only observed in decapitated brains of wild-type mice. These results suggested that cPLA2epsilon is responsible for Ca(2+)-dependent formation of NAPEs in the brain as well as the accumulation of NAPEs and NAEs during ischemia, while other enzyme(s) appeared to be involved in the maintenance of basal NAPE levels. |
