Basic fibroblast growth factor reverses atherosclerotic impairment of human coronary angiogenesis-like responses in vitro

Oxidized Low-Density Lipoprotein Downregulates Endothelial Basic Fibroblast Growth Factor Through a Pertussis Toxin-Sensitive G-Protein Pathway

“…Angiogenesis involves multiple growth factors/cytokines. Like bFGF, 5,6 vascular endothelial growth factor (VEGF) improves collateral-dependent tissue perfusion in hypercholesterolemic rabbits. 23 Previously, we showed that oxLDL downregulates endothelial bFGF without affecting the FGF receptor FGFR-1; the associated reductions in DNA synthesis and capillary-like microtubule growth in arterial explants are reversed by exogenous bFGF, but not by VEGF or transforming growth factor-␤.…”

Oxidized Low Density Lipoproteins in Patients With Transplant-Associated Coronary Artery Disease

“…35,36 Oxidized LDL may also contribute to rapidly progressing coronary atherosclerosis by inducing platelet adhesion, by decreasing the anticoagulant and fibrinolytic capacities of activated endothelium, and by impairing vasodilation and inducing shear stress. [32][33][34] Increased intracellular levels of ferritin 37 or of ␣-tocopherol analogues 38 decreased the extent of endothelial injury elicited by oxidized LDL in vitro, whereas antioxidants protect against progression of atherosclerosis in experimental animals (reviewed in Reference 9).…”

Oxidized Low-Density Lipoproteins Inhibit Endothelial Cell Proliferation by Suppressing Basic Fibroblast Growth Factor Expression

“…4,5 These results support findings that hyperlipidemic impairment of angiogenesis is associated with reduced availability of bFGF and can be corrected by exogenous bFGF. 2,3 The progressive reduction in bFGF expression reflected, in part, accelerated posttranscriptional mRNA degradation. Ox-LDL shortened the bFGF half-life from 24 to Ϸ12 hours after transcription was inhibited by actinomycin D. Sensitive to cyclohexamide, enhanced degradation of bFGF mRNA depended on newly synthesized protein(s).…”

“…2 Cell purity was assessed by uptake of acetylated LDL labeled with 1,1Ј-dioctadecyl-1,3,3,3Ј,3Ј-tetramethylindocarbocyanine perchlorate (Biomedical Technologies), immunocytochemical staining for von Willebrand factor-related antigen with FITC-labeled monoclonal antibody (Incstar), and negative staining for ␣-actin with HHF35 antibody (Enzo). 2,6 More than 98% of the cells exhibited responses typical of cells of endothelial origin. Cells at 8 to 12 passages, maintained in DMEM supplemented with 10% FBS and antibiotics (streptomycin 100 g/mL, penicillin 100 IU/mL, amphotericin B 0.25 g/mL), were used.…”

“…The impairment can be partially reversed by exogenous bFGF. 2,3 Here, we determined whether impairment of proliferative and angiogenic responses induced by ox-LDL is due to suppressed endothelial expression of bFGF or of its receptor, FGFR-1. The effects of bFGF on DNA and total RNA syntheses in the presence of ox-LDL were compared with those of vascular endothelial growth factor (VEGF), an endothelial cell (EC)-specific mitogen and potent angiogenic factor.…”