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dc.contributor.authorElsegood, Caryn
dc.contributor.authorChang, M.
dc.contributor.authorJessup, W.
dc.contributor.authorScholz, G.
dc.contributor.authorHamilton, J.
dc.identifier.citationElsegood, C. and Chang, M. and Jessup, W. and Scholz, G. and Hamilton, J. 2009. Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins. Arteriosclerosis, Thrombosis, and Vascular Biology. 29 (9): pp. 1283-1289.

OBJECTIVE-: Oxidized low-density lipoprotein (oxLDL) induces survival of colony stimulating factor-1 (CSF-1)-dependent macrophages in vitro. Because atherosclerotic lesion-associated macrophages take up large amounts of glucose, we investigated whether, and how, oxLDL promotes glucose uptake and how glucose metabolism regulates oxLDL-induced macrophage survival. METHODS AND RESULTS-: OxLDL-induced macrophage survival required glucose metabolism. OxLDL stimulated 2 phases of glucose uptake, namely acute and chronic, which required PI3K but not MEK1/2 activity. PI3K appeared to regulate glucose transport via glucose transporter affinity and/or mobilization. OxLDL also maintained levels of the prosurvival proteins, Bcl-2 and Bcl-xL, after CSF-1 had been removed through a combination of mechanisms including transcription, translation, and protein stabilization. Significantly, inhibition of glucose metabolism reduced Bcl-2 and Bcl-xL protein levels. MEK1/2 and PI3K activities were also required for oxLDL-induced Bcl-2 and Bcl-xL mRNA upregulation. CONCLUSIONS-: These results suggest that oxLDL enhances macrophage survival in the absence of CSF-1 by inducing PI3K-dependent glucose uptake, which is metabolized to maintain Bcl-2 and Bcl-xL protein levels. © 2009 American Heart Association, Inc.

dc.publisherLippincott Williams & Wilkins
dc.titleGlucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins
dc.typeJournal Article
dcterms.source.titleArteriosclerosis, Thrombosis, and Vascular Biology
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusOpen access via publisher

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