Endothelial Cell Fibrinolysis - Abormal Vldl Influences

Booyse, Francois M.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Heart, Lung, and Blood Institute (NHLBI)
• Type: Research Project (R01)
• Project #: 5R01HL052791-02
• Application #: 2230401
• Study Section: Metabolism Study Section (MET)
• Project Start: 1995-01-01
• Project End: 1998-12-31
• Budget Start: 1996-01-01
• Budget End: 1996-12-31
• Support Year: 2
• Fiscal Year: 1996

Institution

• Name: University of Alabama Birmingham
• Department: Internal Medicine/Medicine
• Type: Schools of Medicine
• DUNS #: 004514360
• City: Birmingham
• State: AL
• Country: United States
• Zip Code: 35294

Publications

Tabengwa, E M; Benza, R L; Grenett, H E et al. (2000) Hypertriglyceridemic VLDL downregulates tissue plasminogen activator gene transcription through cis-repressive region(s) in the tissue plasminogen activator promoter in cultured human endothelial cells. Arterioscler Thromb Vasc Biol 20:1675-81

Benza, R L; Grenett, H E; Bourge, R C et al. (1998) Gene polymorphisms for plasminogen activator inhibitor-1/tissue plasminogen activator and development of allograft coronary artery disease. Circulation 98:2248-54

Grenett, H E; Benza, R L; Fless, G M et al. (1998) Genotype-specific transcriptional regulation of PAI-1 gene by insulin, hypertriglyceridemic VLDL, and Lp(a) in transfected, cultured human endothelial cells. Arterioscler Thromb Vasc Biol 18:1803-9

Li, X N; Grenett, H E; Benza, R L et al. (1997) Genotype-specific transcriptional regulation of PAI-1 expression by hypertriglyceridemic VLDL and Lp(a) in cultured human endothelial cells. Arterioscler Thromb Vasc Biol 17:3215-23

Li, X N; Koons, J C; Benza, R L et al. (1996) Hypertriglyceridemic VLDL decreases plasminogen binding to endothelial cells and surface-localized fibrinolysis. Biochemistry 35:6080-8