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Proteomic analysis of mitochondria in APOE transgenic mice and in response to an ischemic challenge

James, Rachel, Searcy, James L, Bihan, Thierry Le, Martin, Sarah F, Gliddon, Catherine M, Povey, Joanne, Deighton, Ruth F, Kerr, Lorraine E, McCulloch, James and Horsburgh, Karen 2011. Proteomic analysis of mitochondria in APOE transgenic mice and in response to an ischemic challenge. Journal of Cerebral Blood Flow and Metabolism 32 (1) , pp. 164-176. 10.1038/jcbfm.2011.120

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Apolipoprotein E (APOE)-ɛ4 is associated with a deleterious outcome after ischemic brain injury, which may involve abnormal regulation of mitochondrial function. We have assessed the mitochondrial proteomic response of APOE-ɛ3 and APOE-ɛ4 transgenic mice to transient global ischemic injury in the hippocampus. A genotype-dependent increase in ApoE levels in mitochondria was observed after ischemia, with APOE-ɛ4 mice showing significantly greater increases than APOE-ɛ3 mice. Quantitative analysis of the mitochondria-enriched fractions was performed using liquid-chromatography mass spectrometry coupled to label-free analysis. Of the 1,067 identified proteins, 274 were mitochondria associated. Mitochondrial protein expression was significantly different between genotypes under basal conditions as well as in response to global ischemia. A total of 12 mitochondrial proteins (including respiratory chain proteins NDUFA11, NDUFS3, NDUF5B, ATP5J, as well as ETFA, CYB5B, ATP6V1A, HSPA1B, OXR1, GLUL, IARS2, and PHYHIPL) were significantly altered with respect to genotype, global ischemia, or their interaction (P<0.01). A compelling interactome, created using proteins found to be significantly modulated by global ischemia (P<0.05), involved proteins that regulate energy production and oxidative stress. Thus, APOE genotype has a differential effect on the mitochondrial protein expression in the absence and presence of an injury, which may underlie the differing genotype susceptibility.

Item Type: Article
Date Type: Published Online
Status: Published
Schools: Medicine
Publisher: Nature Publishing Group: Open Access Hybrid Model Option B
ISSN: 0271-678X
Date of Acceptance: 18 July 2011
Last Modified: 09 Jul 2018 13:01

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