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Cell Growth & Differentiation, Vol 9, Issue 9 723-730, Copyright © 1998 by American Association of Cancer Research


ARTICLES

Basic fibroblast growth factor-induced decrease in type I collagen gene transcription is mediated by B-myb

KE Kypreos, MA Nugent and GE Sonenshein
Department of Biochemistry, Boston University School of Medicine, Massachusetts 02118, USA.

Basic fibroblast growth factor (bFGF), a member of the fibroblast growth factor family, potently induces increased vascular smooth muscle cell (SMC) proliferation and decreased expression of type I collagen. Recently, our laboratory demonstrated that, in bovine vascular SMCs, expression of B-myb, a member of the myb gene family, is dependent upon cellular growth state and that B-myb decreases alpha1(I) collagen promoter activity in transient transfection assays. Nuclear run-off analysis indicated that the decrease in alpha1(I) collagen mRNA level seen upon bFGF treatment was due to a decline in the rate of alpha1(I) procollagen gene transcription. Thus, we investigated the potential role of B-Myb in the down-regulation of type I collagen gene expression by bFGF. Using Northern blot analysis, we found that bFGF treatment of bovine aortic SMCs caused an increase in B-myb mRNA levels. Ectopic expression of B-myb decreased endogenous alpha1(I) collagen mRNA levels. Importantly, introduction of a B-myb antisense oligonucleotide prevented the drop in the alpha1(I) collagen mRNA levels seen upon treatment with bFGF. Together, these results indicate that B-myb mediates signals leading to the decreased rate of alpha1(I) collagen gene transcription caused by bFGF.


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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1998 by the American Association of Cancer Research.