AI Article Synopsis
- Group IVA phospholipase A2 (IVA-PLA2) generates arachidonate and is involved in inflammation.
- Mice lacking IVA-PLA2 showed reduced liver damage and cell death after exposure to carbon tetrachloride (CCl4) but did not impact lipid peroxidation levels.
- Higher levels of LC3-II in IVA-PLA2-deficient cells indicated increased autophagosome formation, suggesting that IVA-PLA2 might promote CCl4-induced cell death by inhibiting autophagy in liver cells.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.bbrc.2016.01.186 | DOI Listing |
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