Study on the differential proteomics of rat hippocampal mitochondria during deep hypothermic circulatory arrest

This study aimed to investigate the effect of deep hypothermic circulatory arrest (DHCA) on rat hippocampal mitochondrial protein expression and its differential proteomics, and explore the potential mechanisms behind the effect.

We used internal jugular vein reflux and tail artery perfusion methods to establish the rat cardiopulmonary bypass (CPB) model. Rats were dissected to obtain the hippocampus, and the hippocampal mitochondria were purified. The mitochondrial morphology and the mitochondrial marker cytochrome C oxidase (COX) qualitatively examined via transmission electron microscopy and western-blot analysis, respectively. The qualified samples were subjected to isobaric tags for relative and absolute quantification (iTRAQ); we then established the CPB model again to obtain the rat hippocampus for cryoultramicrotomy, and used immunofluorescent double staining technique to qualitatively and semi-quantitatively verify two representative differentially expressed proteins.

By searching the Mascot 2.2 database, 29 differentially expressed proteins were obtained with statistical significance, including 21 known proteins and 8 unknowns. The expression level of COX and monoacylglycerol lipase did not change significantly (P>0.05) during the hyperacute phase; however, their intracellular localizations were altered.

DHCA induced the differential expression of 29 rat hippocampal mitochondrial proteins, some of which had altered intracellular localization. We speculated that the localized alteration of these proteins is one of the neuroprotection mechanisms that occurs during DHCA.