AI Article Synopsis
- Dysregulated cholesterol levels in the liver can lead to nonalcoholic steatohepatitis and chronic liver damage.
- The study investigated how excess free cholesterol affects lipid droplets in liver cells, causing them to fuse and degrade protective proteins like perilipin 2.
- The binding of apolipoprotein B 100 to these lipid droplets relies on Rab18 protein activity, suggesting that lipid droplets are significant targets for cholesterol toxicity in liver cells.
Article Abstract
Dysregulated hepatic cholesterol homeostasis with free cholesterol accumulation in the liver is relevant to the pathogenesis of nonalcoholic steatohepatitis, contributing to the chronicity of liver toxicity. Here we examined the effect of free cholesterol accumulation on the morphology and biochemical properties of lipid droplets (LDs) in cultured hepatocytes. Acute free cholesterol accumulation induced the fusion of LDs, followed by degradation of the coat protein of LDs, perilipin 2 (PLIN2; also called adipophilin or adipose differentiation-related protein), and association of apolipoprotein B 100 (ApoB 100) to LDs. The degradation of PLIN2 was inhibited by inhibitors of ubiquitination, autophagy, and protein synthesis. The results indicate that association of ApoB 100 with LDs is dependent on the activity of low-molecular weight GTP-binding protein Rab18 and highlight the role of LDs as targets of free cholesterol toxicity in hepatocytes.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5170862 | PMC |
| http://dx.doi.org/10.1091/mbc.E15-10-0730 | DOI Listing |
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