The purpose of Core B is to facilitate research and stimulate collaboration between the individual projects. Specifically, Core B will offer the following services: 1. Lipoprotein isolation and characterization 2. Plasma lipoprotein analysis 3. Plasma lipid analysis 4. Labeling of proteins/lipoproteins with radioisotopes and fluorescent dyes 5. HDL remnant particle purification and characterization 6. Production of replication-defective adenoviral vectors and helper-dependent adenoviral vectors 7. Purification of total SAA and SAA isoforms 8. Isoelectric focusing Centralization of these facilities will permit an efficient use of resources for the Program and experienced technical staff will provide optimal quality control and standardization across Projects.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL086670-04
Application #
8049661
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2010-04-01
Budget End
2011-03-31
Support Year
4
Fiscal Year
2010
Total Cost
$215,850
Indirect Cost
Name
University of Kentucky
Department
Type
DUNS #
939017877
City
Lexington
State
KY
Country
United States
Zip Code
40506
Kim, Myung-Hee; de Beer, Maria C; Wroblewski, Joanne M et al. (2016) Impact of individual acute phase serum amyloid A isoforms on HDL metabolism in mice. J Lipid Res 57:969-79
Webb, Nancy R; De Beer, Maria C; Wroblewski, Joanne M et al. (2015) Deficiency of Endogenous Acute-Phase Serum Amyloid A Protects apoE-/- Mice From Angiotensin II-Induced Abdominal Aortic Aneurysm Formation. Arterioscler Thromb Vasc Biol 35:1156-65
Ji, Ailing; Wroblewski, Joanne M; Webb, Nancy R et al. (2014) Impact of phospholipid transfer protein on nascent high-density lipoprotein formation and remodeling. Arterioscler Thromb Vasc Biol 34:1910-6
De Beer, Maria C; Wroblewski, Joanne M; Noffsinger, Victoria P et al. (2014) Deficiency of endogenous acute phase serum amyloid A does not affect atherosclerotic lesions in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 34:255-61
Meyer, Jason M; Ji, Ailing; Cai, Lei et al. (2014) Minimally oxidized LDL inhibits macrophage selective cholesteryl ester uptake and native LDL-induced foam cell formation. J Lipid Res 55:1648-56
Tang, Tao; Thompson, Joel C; Wilson, Patricia G et al. (2013) Decreased body fat, elevated plasma transforming growth factor-? levels, and impaired BMP4-like signaling in biglycan-deficient mice. Connect Tissue Res 54:5-13
Meyer, Jason M; Graf, Gregory A; van der Westhuyzen, Deneys R (2013) New developments in selective cholesteryl ester uptake. Curr Opin Lipidol 24:386-92
de Beer, Maria C; Wroblewski, Joanne M; Noffsinger, Victoria P et al. (2013) The Impairment of Macrophage-to-Feces Reverse Cholesterol Transport during Inflammation Does Not Depend on Serum Amyloid A. J Lipids 2013:283486
Kim, Myung-Hee; de Beer, Maria C; Wroblewski, Joanne M et al. (2013) SAA does not induce cytokine production in physiological conditions. Cytokine 61:506-12
Cai, Lei; Wang, Zhen; Meyer, Jason M et al. (2012) Macrophage SR-BI regulates LPS-induced pro-inflammatory signaling in mice and isolated macrophages. J Lipid Res 53:1472-81

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