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Basic fibroblast growth factor-induced decrease in type I collagen gene transcription is mediated by B-myb
K E Kypreos1, M A Nugent, G E Sonenshein
1Department of Biochemistry, Boston University School of Medicine, Massachusetts 02118, USA.
Cell Growth & Differentiation : the Molecular Biology Journal of the American Association for Cancer Research
|September 29, 1998
Summary
Basic fibroblast growth factor (bFGF) increases vascular smooth muscle cell proliferation by upregulating B-myb. This B-myb then decreases type I collagen gene transcription, revealing a key molecular mechanism in vascular remodeling.
Area of Science:
- Molecular Biology
- Cell Biology
- Cardiovascular Research
Background:
- Basic fibroblast growth factor (bFGF) promotes vascular smooth muscle cell (SMC) proliferation and reduces type I collagen expression.
- B-myb gene expression is linked to cellular growth state in bovine vascular SMCs.
- bFGF treatment decreases alpha1(I) collagen gene transcription in SMCs.
Purpose of the Study:
- To investigate the role of B-myb in bFGF-induced down-regulation of type I collagen gene expression in vascular SMCs.
Main Methods:
- Northern blot analysis to assess B-myb mRNA levels.
- Ectopic expression of B-myb to evaluate its effect on collagen mRNA.
- Use of B-myb antisense oligonucleotides to block bFGF-induced changes.
Main Results:
- bFGF treatment increased B-myb mRNA levels in bovine aortic SMCs.
- Overexpression of B-myb led to decreased endogenous alpha1(I) collagen mRNA.
- B-myb antisense oligonucleotides inhibited the bFGF-induced reduction in alpha1(I) collagen mRNA.
Conclusions:
- B-myb mediates the bFGF-induced decrease in type I collagen gene transcription.
- This study elucidates a novel pathway involving B-myb in vascular cell regulation by bFGF.