PRELIMINARY DATA ON THE AGE-DEPENDENT DECREASE IN BASIC FIBROBLAST GROWTH-FACTOR AND PLATELET-DERIVED GROWTH-FACTOR IN THE HUMAN VEIN WALL AND IN THEIR INFLUENCE ON CELL-PROLIFERATION

Citation
I. Drubaix et al., PRELIMINARY DATA ON THE AGE-DEPENDENT DECREASE IN BASIC FIBROBLAST GROWTH-FACTOR AND PLATELET-DERIVED GROWTH-FACTOR IN THE HUMAN VEIN WALL AND IN THEIR INFLUENCE ON CELL-PROLIFERATION, Gerontology, 44(1), 1998, pp. 9-14
Citations number
27
Categorie Soggetti
Geiatric & Gerontology
Journal title
ISSN journal
0304324X
Volume
44
Issue
1
Year of publication
1998
Pages
9 - 14
Database
ISI
SICI code
0304-324X(1998)44:1<9:PDOTAD>2.0.ZU;2-A
Abstract
The roles of basic fibroblast growth factor (bFGF) and platelet-derive d growth factor (PDGF) in vein disease and aging were investigated. Sm ooth muscle cells from human saphenous veins were cultured. The age de pendence of bFGF and PDGF activation of the smooth muscle cell prolife ration was determined, and the bFGF and PDGF contents in vein wall hom ogenates were measured by an enzyme-linked sorbent assay. There were m orphological alterations in the cells with more polygonal and polynucl eated cells in cultures from aged donors, similar to those observed in vitro in aged cell cultures. Some cultures did not reach confluency a fter the tenth passage, suggesting early decay of the cultures from di seased veins. bFGF and PDGF stimulated the proliferation of the vein s mooth muscle cells, but only in cultures treated with hyaluronidase. T his stimulation decreased with the age of the donor. The amount of the two growth factors in human vein walls decreased with donor age. The amount of bFGF decreased faster (slope: 3.3138 ng/mg DNA/year) than th at of PDGF (slope: 1.021 ng/mg DNA/year). This results in an age-depen dent change in the bFGF/PDGF ratio from 4 mol/mol at the age of 20 yea rs to 1 mol/mol at the age of 80. These growth factors also modulate t he synthesis of extracellular matrix components. The continuous change in the bFGF/PDGF ratio may alter the composition of the extracellular matrix of the vein wall during aging and thus its susceptibility to v aricose disease.