Nicotine regulates basic fibroblastic growth factor and transforming growth factor beta1 production in endothelial cells

Autor: Marco Lucarelli, Paolo Sapienza, Sigfrido Scarpa, Luciana Santoro-D'Angelo, Valentina Corvino, Alessandra Cucina, Roberto Strom, Valeria Borrelli, Antonino Cavallaro
Rok vydání: 1999
Předmět:
Arteriosclerosis
medicine.medical_treatment
aortic endothelial cells
Stimulation
Cell Count
Biochemistry
Polymerase Chain Reaction
Nicotine
chemistry.chemical_compound
Transforming Growth Factor beta
Settore BIO/13 - BIOLOGIA APPLICATA
Mitogenic activity
Aorta
medicine.diagnostic_test
nicotine
bFGF
TGFb
endothelial cells
Antibodies
Monoclonal
TGFbeta
Fibroblast Growth Factor 2
Cell Division
medicine.drug
medicine.medical_specialty
medicine.drug_class
Cell Survival
Blotting
Western
Biophysics
Biology
Monoclonal antibody
Western blot
Internal medicine
medicine
Animals
RNA
Messenger
Molecular Biology
Dose-Response Relationship
Drug
Growth factor
Muscle
Smooth
Cell Biology
DNA
Endocrinology
chemistry
Culture Media
Conditioned
Cattle
Endothelium
Vascular
Mitogens
Thymidine
Transforming growth factor
Zdroj: Biochemical and biophysical research communications. 257(2)
ISSN: 0006-291X
Popis: Nicotine, a constituent of cigarette smoking, may induce atherosclerosis through the production of growth factors. The pattern of bFGF and TGF beta1 production and release by bovine aortic endothelial cells (EC) stimulated with nicotine (from 6 x 10(-4) to 6 x 10(-8) M) was studied. EC viability and count were assessed. The presence of bFGF and TGF beta1 in serum-free conditioned media was determined by the inhibition antibody-binding assay and Western blot analysis. Mitogenic activity of nicotine on EC was also determined. Polymerase chain reaction (PCR) was used to study the expression of bFGF and TGF beta1. The bFGF release after nicotine stimulation was greater than controls, whereas TGF beta1 release was lower. At a nicotine concentration of 6 x 10(-6) M we noted the greatest mitogenic activity. The addition of monoclonal antibody anti-bFGF decreased the tritiated thymidine uptake of EC exposed to nicotine but the addition of monoclonal antibody anti-TGF beta1 had no significant effect. bFGF mRNA expression was significantly higher in EC exposed to nicotine than in controls, whereas TGF beta1 mRNA expression was not modified. From these data we concluded that nicotine regulates bFGF production and release and TGF beta1 release and may have a key role in the development and progression of atherosclerosis.
Databáze: OpenAIRE
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