Publication: Transforming growth factor-01 gene and protein expression associated with atherogenesis of cholesterol-fed rabbits
Loading...
Date
2000
Authors
Chen, Y.L. ; Wu, H.W. ; Jlang, M.J.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Transforming growth factor-l31 (TGF-l31) has
been shown to modulate both cell proliferation and the
synthesis of extracellular matrix by vascular cells. This
study was aimed to establish the temporal correlation
between TGF-l31 expression, the expression of the
extracellular matrix protein fibronectin, and plaque
development during atherogenesis of hypercholesterolemic
rabbits. New Zealand White rabbits
were fed with 2% cholesterol-supplemented chow for 1
week, 2 weeks, 3 weeks or 6 weeks. TGF-l31 mRNA and
protein expression was examined in serial sections of
aorta by in situ hybridization and immunohistochemistry.
Fibronectin expression was examined by
immunohistochemistry. In the control and l-week
feeding group, the expression of TGF-l31 mRNA and
protein was not apparent. In 2-week feeding group,
intimal thickening was detected in which TGF-B1
mRNA and protein were not clearly observed, either.
The 3-week and 6-week feeding groups exhibited fatty
streaks in which TGF-l31 mRNA and protein expression
markedly increased as feeding proceeded. Cell typespecific
staining indicated that TGF-l31 was expressed
by macrophages as well as smooth muscle cells of the
fatty streaks. Immunostaining of fibronectin detected
low expression levels in control, l-week and 2-week
feeding groups with pronounced upregulation in the
thickened intima and the proximal media in 3-week and
6-week feeding groups. These results implicate a role for
TGF-l31 in modulating fatty streak formation and the
synthesis of extracellular protein fibronectin during
plaque development.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.