Regulation by Basic Fibroblast Growth Factor of Glycosaminoglycan Biosynthesis in Cultured Vascular Endothelial Cells

1995 ◽  
Vol 49 (3) ◽  
pp. 268-276 ◽  
Author(s):  
Toshiyuki Kaji ◽  
Syouichi Hiraga ◽  
Susumu Ohkawara ◽  
Miho Inada ◽  
Chika Yamamoto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Fibroblast Growth

scholarly journals Basic fibroblast growth factor is an extracellular matrix component required for supporting the proliferation of vascular endothelial cells and the differentiation of PC12 cells.

1989 ◽  
Vol 109 (2) ◽  
pp. 823-831 ◽  
Author(s):  
S Rogelj ◽  
M Klagsbrun ◽  
R Atzmon ◽  
M Kurokawa ◽  
A Haimovitz ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Neurite Outgrowth ◽  
Fibroblast Growth Factor ◽  
Pc12 Cells ◽  
Basic Fibroblast Growth Factor ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Fibroblast Growth

Vascular endothelial cells (ECs) seeded sparsely on extracellular matrix (ECM) will proliferate in the absence of exogenous basic fibroblast growth factor (bFGF). This ECM will also stimulate neurite outgrowth in PC12 cells in the absence of exogenous growth factors. We have previously shown that bFGF is found in subendothelial ECM (Vlodavsky, I., J. Folkman, R. Sullivan, R. Fridman, R. Ishai-Michaeli, J. Sasse, and M. Klagsburn. 1987. Proc. Natl. Acad. Sci. USA. 84:2292-2296) and in basement membranes (Folkman, J., M. Klagsburn, J. Sasse, M. Wadzinski, D. Ingber, and I. Vlodavsky. 1988. Am. J. Pathol. 130:393-400). The actual requirement of ECM-associated bFGF for the growth of ECs and differentiation of PC12 cells was shown in two ways. First, polyclonal anti-bFGF antibodies added to subendothelial ECM inhibited both EC proliferation and PC12 neurite outgrowth. Secondly, PF-HR-9 cells, which do not synthesize bFGF and which produce an ECM not permissive for EC proliferation and PC12 neurite outgrowth, were transfected with bFGF cDNA. PF-HR-9 cells transfected with bFGF, but not with the dominant selectable marker SV2-neomycin, were found to express bFGF and to produce an ECM which did support both EC proliferation and PC12 differentiation. The ECM-mediated stimulatory effects were inhibited by anti-bFGF antibodies but not by anti-nerve growth factor antibodies or nonimmune rabbit IgG. These results indicate that bFGF associated with ECM is a required ECM component for ECM-mediated cell proliferation and differentiation.

scholarly journals Expression of the urokinase receptor in vascular endothelial cells is stimulated by basic fibroblast growth factor.

1991 ◽  
Vol 113 (5) ◽  
pp. 1193-1201 ◽  
Author(s):  
P Mignatti ◽  
R Mazzieri ◽  
D B Rifkin
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Plasminogen Activator Inhibitor ◽  
Vascular Endothelial ◽  
Fibroblast Growth ◽  
Single Chain

Basic fibroblast growth factor, a potent angiogenesis inducer, stimulates urokinase (uPA) production by vascular endothelial cells. In both basic fibroblast growth factor-stimulated and -nonstimulated bovine capillary endothelial and human umbilical vein endothelial cells single-chain uPA binding is mediated by a membrane protein with a Mr of 42,000. Exposure of bovine capillary or endothelial human umbilical vein endothelial cells to pmolar concentrations of basic fibroblast growth factor results in a dose-dependent, protein synthesis-dependent increase in the number of membrane receptors for uPA (19,500-187,000) and in a parallel decrease in their affinity (KD = 0.144-0.790 nM). With both cells, single-chain uPA binding is competed by synthetic peptides whose sequence corresponds to the receptor-binding sequence in the NH2-terminal domain of uPA. Exposure of bovine capillary endothelial cells to transforming growth factor beta 1, which inhibits uPA production and upregulates type 1 plasminogen activator inhibitor, the major endothelial cell plasminogen activator inhibitor, has no effect on uPA receptor levels. These results show that basic fibroblast growth factor, besides stimulating uPA production by vascular endothelial cells, also increases the production of receptors, which modulates their capacity to focalize this enzyme on the cell surface. This effect may be important in the degradative processes that occur during angiogenesis.

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