Abstract

This proposal addresses the thesis that chronic inflammatory diseases - common in an ageing population - accelerates the development of atherosclerosis. During the acute phase response, serum amyloid A protein (A-5A-A>, an apolipoprotein, increases 1,000 fold and becomes a major component of high density lipoprotein (HDL). In spite of intense modern interest in the HDL particle, the teleological role of this alteration of HDL apolipoprotein composition during inflammation is unknown. The investigators propose that A-SAA mediate the remodelling of HDL to accommodate a modified physiological requirement for this particle during

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
1R01AG010886-01A2
Application #
2052116
Study Section
Pathology A Study Section (PTHA)
Project Start
1994-08-10
Project End
1999-07-31
Budget Start
1994-08-10
Budget End
1995-07-31
Support Year
1
Fiscal Year
1994
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