Wong, Heng Yeng and Langlotz, Monika and Gan-Schreier, Hongying and Xu, Weihong and Staffer, Simone and Tuma-Kellner, Sabine and Liebisch, Gerhard and Merle, Uta and Chamulitrat, Walee (2021) Constitutive oxidants from hepatocytes of male iPLA2 beta-null mice increases the externalization of phosphatidylethanolamine on plasma membrane. FREE RADICAL RESEARCH, 55 (6). pp. 625-633. ISSN 1071-5762, 1029-2470
Full text not available from this repository. (Request a copy)Abstract
We have found that group VIA calcium-independent phospholipase A2 (iPLA2 beta) has specificity for hydrolysis of phosphatidylethanolamine (PE) in mouse livers. Phospholipids (PLs) are transported to plasma membrane and some PLs including PE are externalized to maintain membrane PL asymmetry. Here we demonstrated that hepatocytes of iPLA2 beta-null (KO) mice showed an increase in PE containing palmitate and oleate. We aimed to examine whether externalization of PE on the outer leaflets could be affected by iPLA2 beta deficiency and its modulation by reactive oxygen species (ROS) or apoptosis. As duramycin has high affinity to PE, we used duramycin conjugated with biotin (DLB) and streptavidin 488 as a probe for detection of externalized PE. Compared to WT, naive KO hepatocytes showed an increase in both PE externalization and ROS generation. These events were observed in male but not in female KO mice. Hydrogen peroxide or menadione treatment enhanced PE externalization to the same extent for both male/female WT and KO hepatocytes. By indirect immunofluorescence, DLB-streptavidin staining was observed as small punctuated spots on the cell surface of menadione-treated KO hepatocytes. Unlike the reported PS externalization, CD95/FasL treatment did not lead to any increase in PE externalization, and iPLA2 beta deficiency-dependent PE externalization was also not correlated with apoptosis. Thus, constitutive (but not induced) ROS generation in iPLA2 beta-deficient hepatocytes leads to PE externalization observed only in male mice. Such PE externalization may imply detrimental effects regarding further oxidation of PE fatty acids and the binding with pathogens on the outer leaflets of hepatocyte plasma membrane.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | LIPID-PEROXIDATION; OXIDATIVE DAMAGE; PHOSPHATIDYLSERINE; APOPTOSIS; DEFICIENCY; EXPOSURE; SURFACE; PHOSPHATIDYLCHOLINE; REDISTRIBUTION; SPHINGOMYELIN; hepatocytes; phospholipid asymmetry; reactive oxygen species; outer leaflets |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 08 Sep 2022 14:43 |
| Last Modified: | 08 Sep 2022 14:43 |
| URI: | https://pred.uni-regensburg.de/id/eprint/46878 |
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