Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins
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...
| Main Authors: | , , , , |
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| Format: | Journal Article |
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Lippincott Williams & Wilkins
2009
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| Online Access: | http://hdl.handle.net/20.500.11937/21809 |
| _version_ | 1848750693869944832 |
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| author | Elsegood, Caryn Chang, M. Jessup, W. Scholz, G. Hamilton, J. |
| author_facet | Elsegood, Caryn Chang, M. Jessup, W. Scholz, G. Hamilton, J. |
| author_sort | Elsegood, Caryn |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | 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. |
| first_indexed | 2025-11-14T07:40:54Z |
| format | Journal Article |
| id | curtin-20.500.11937-21809 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-14T07:40:54Z |
| publishDate | 2009 |
| publisher | Lippincott Williams & Wilkins |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-218092017-09-13T13:54:25Z Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins Elsegood, Caryn Chang, M. Jessup, W. Scholz, G. Hamilton, J. 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. 2009 Journal Article http://hdl.handle.net/20.500.11937/21809 10.1161/ATVBAHA.108.180778 Lippincott Williams & Wilkins unknown |
| spellingShingle | Elsegood, Caryn Chang, M. Jessup, W. Scholz, G. Hamilton, J. Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins |
| title | Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins |
| title_full | Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins |
| title_fullStr | Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins |
| title_full_unstemmed | Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins |
| title_short | Glucose metabolism is required for oxidized LDL-induced macrophage survival: Role of PI3K and Bcl-2 family proteins |
| title_sort | glucose metabolism is required for oxidized ldl-induced macrophage survival: role of pi3k and bcl-2 family proteins |
| url | http://hdl.handle.net/20.500.11937/21809 |