| First Author | Ishihara K | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 471 |
| Issue | 1 | Pages | 15-20 |
| PubMed ID | 26850849 | Mgi Jnum | J:233325 |
| Mgi Id | MGI:5781261 | Doi | 10.1016/j.bbrc.2016.01.186 |
| Citation | Ishihara K, et al. (2016) Group IVA phospholipase A(2) deficiency prevents CCl4-induced hepatic cell death through the enhancement of autophagy. Biochem Biophys Res Commun 471(1):15-20 |
| abstractText | Group IVA phospholipase A2 (IVA-PLA2), which generates arachidonate, plays a role in inflammation. IVA-PLA2-deficiency reduced hepatotoxicity and hepatocyte cell death in mice that received a single dose of carbon tetrachloride (CCl4) without any inhibitory effects on CCl4-induced lipid peroxidation. An immunoblot analysis of extracts from wild-type mouse- and IVA-PLA2 KO mouse-derived primary hepatocytes that transiently expressed microtubule-associated protein 1 light chain 3B (LC3) revealed a higher amount of LC3-II, a typical index of autophagosome formation, in IVA-PLA2-deficient cells, suggesting the enhancement of constitutive autophagy. IVA-PLA2 may promote CCl4-induced cell death through the suppression of constitutive autophagy in hepatocytes. |
