Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
5R01AG010886-03
Application #
2052118
Study Section
Pathology A Study Section (PTHA)
Program Officer
Finkelstein, David B
Project Start
1994-08-10
Project End
1999-07-31
Budget Start
1996-08-01
Budget End
1997-07-31
Support Year
3
Fiscal Year
1996
Total Cost
Indirect Cost

  Institution

Name
University of Kentucky
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
832127323
City
Lexington
State
KY
Country
United States
Zip Code
40506

  Publications

Chiba, Tsuyoshi; Chang, Mary Y; Wang, Shari et al. (2011) Serum amyloid A facilitates the binding of high-density lipoprotein from mice injected with lipopolysaccharide to vascular proteoglycans. Arterioscler Thromb Vasc Biol 31:1326-32
Suzuki, Masashi; Pritchard, David K; Becker, Lev et al. (2010) High-density lipoprotein suppresses the type I interferon response, a family of potent antiviral immunoregulators, in macrophages challenged with lipopolysaccharide. Circulation 122:1919-27
de Beer, F C; Connell, P M; Yu, J et al. (2000) HDL modification by secretory phospholipase A(2) promotes scavenger receptor class B type I interaction and accelerates HDL catabolism. J Lipid Res 41:1849-57
Kindy, M S; de Beer, M C; Yu, J et al. (2000) Expression of mouse acute-phase (SAA1.1) and constitutive (SAA4) serum amyloid A isotypes: influence on lipoprotein profiles. Arterioscler Thromb Vasc Biol 20:1543-50
Kindy, M S; de Beer, F C (1999) A mouse model for serum amyloid A amyloidosis. Methods Enzymol 309:701-16
Leitinger, N; Watson, A D; Hama, S Y et al. (1999) Role of group II secretory phospholipase A2 in atherosclerosis: 2. Potential involvement of biologically active oxidized phospholipids. Arterioscler Thromb Vasc Biol 19:1291-8
Ivandic, B; Castellani, L W; Wang, X P et al. (1999) Role of group II secretory phospholipase A2 in atherosclerosis: 1. Increased atherogenesis and altered lipoproteins in transgenic mice expressing group IIa phospholipase A2. Arterioscler Thromb Vasc Biol 19:1284-90
Hosoai, H; Webb, N R; Glick, J M et al. (1999) Expression of serum amyloid A protein in the absence of the acute phase response does not reduce HDL cholesterol or apoA-I levels in human apoA-I transgenic mice. J Lipid Res 40:648-53
Pruzanski, W; Stefanski, E; de Beer, F C et al. (1998) Lipoproteins are substrates for human secretory group IIA phospholipase A2: preferential hydrolysis of acute phase HDL. J Lipid Res 39:2150-60
Webb, N R; de Beer, M C; van der Westhuyzen, D R et al. (1997) Adenoviral vector-mediated overexpression of serum amyloid A in apoA-I-deficient mice. J Lipid Res 38:1583-90

Showing the most recent 10 out of 15 publications