Proteomic analysis of changes in protein expression in liver mitochondria in apoE knockout mice

The involvement of both apolipoprotein E (apoE) and mitochondria in lipid metabolism is widely recognized, however there is surprisingly scarce data about the putative mitochondrial action(s) of this protein. The aim of the study was to screen the alterations in liver mitochondrial proteome caused by apoE deficiency. We applied 2DE-LC-MS/MS methodology to investigate the changes in liver mitochondrial protein expression in 6-months old apoE−/− mice as compared to C57BL/6J controls. ApoE−/−, but not C57BL/6J mice developed visible atherosclerotic changes in aorta and mild, diffuse steatosis of the liver. Collectively, 18 differentially expressed proteins were identified in mitochondria, related to apoptosis, antioxidant and detoxifying mechanisms of mitochondria, as well as lipid metabolism and transport. In conclusion, differential proteomic approach revealed several lines of proteomic evidence that mitochondrial function in the liver of apoE−/− mice could be altered as a result of overlapping of pathological and compensatory changes in expression of proteins.

Graphical AbstractFigure optionsDownload high-quality image (102 K)Download as PowerPoint slideResearch Highlights
► Atherosclerosis in apoE−/− mice is associated with moderate, diffuse steatosis of the liver.
► Analysis of mitoproteome shows the presence of apolipoprotein E in liver mitochondria.
► Upregulation of major urinary protein is eminent change in apoE−/− mice mitochondria.
► Upregulation of glyoxalase 2 may serve as important compensatory mechanism in liver of apoE−/− mice.
► Proteomic data highlight potentially important targets for future pharmacotherapy of fatty liver.