Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
Volume 1867, Issue 12, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.bbalip.2022.159222
Keywords
N -acylethanolamine; N -acyl-phosphatidylethanolamine; N -acyltransferase; Brain ischemia; Endocannabinoid; Phospholipase A (2)
Funding
- Japan Society for the Promotion of Science [JP19K23828, JP20H05691, JP19K07353]
- Strategic Research Support Fund of Kagawa University Research Promotion Program 2021 (KURPP)
- Charitable Trust MIU Foundation Memorial Fund
- Takeda Science Foundation
- AMED-CREST [JP22gm1210013]
- Japan Agency for Medical Research and Development
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N-Acyl-phosphatidylethanolamines (NAPEs) and their bioactive metabolites (NAEs) accumulate during ischemia. The enzyme cPLA(2)epsilon is responsible for the formation of NAPEs during ischemia.
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 A(2)epsilon(cPLA(2)epsilon, 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 cPLA(2)epsilon using cPLA(2)epsilon-deficient (Pla2g4e(-/-)) mice. As analyzed with brain homogenates of wild-type mice, the age dependency of Ca2+-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 cPLA(2)epsilon is responsible for Ca2+--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.
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