Transactivation of EGF receptor induced by angiotensin II regulates fibronectin and TGF-β gene expression via transcriptional and post-transcriptional mechanisms View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2000

AUTHORS

Hiroaki Matsubara , Yasutaka Moriguchi , Yasukiyo Mori , Hiroya Masaki , Yoshiaki Tsutsumi , Yasunobu Shibasaki , Yoko Uchiyama-Tanaka , Schoichiro Fujiyama , Yoko Koyama , Atsuko Nose-Fujiyama , Satoshi Iba , Eriko Tateishi , Toshiji Iwasaka

ABSTRACT

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of growth factor, and recent evidence indicates transactivation of epidermal growth factor receptor (EGF-R) by G protein-coupled receptors. Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and TGF-β in cardiac fibroblasts. Ang II stimulated fibronectin mRNA levels dose-dependently with a maximal increase (∼ 5-fold) observed after 12 h of incubation. Ang II-, or calcium ionophore-induced fibronectin synthesis was completely abolished by tyrosine kinase inhibitors and intracellular Ca2+ chelating agents. Ang II-induced fibronectin mRNA was not affected by PKC inhibitors or PKC depletion, whereas specific inhibition of EGF-R function by a dominant negative EGF-R mutant and tyrphostin AG1478 abolished induction of fibronectin mRNA. We isolated the rat fibronectin gene including the 5’-flanking region and found that the AP-1 binding site present in the promoter region was responsible for the Ang II responsiveness of this gene. Gel retardation assay revealed the binding of nuclear protein to the AP-1 site, which was supershifted with anti-c-fos and anti-c-jun but not anti-ATF-2 antibodies. Conditioned medium from Ang II-treated cells contained TGF-β bioactivity and addition of neutralizing TGF-β antibody modestly (46%) inhibited induction of fibronectin. Ang II-induced synthesis of TGF- β was also abolished by inhibition of EGF-R function. The effect of TGF-β was exerted by stabilizing fibronectin mRNA without affecting the promoter activity and required de novo protein synthesis. We concluded that Ang II-induced expression of fibronectin and TGF- β is mediated by downstream signaling of EGF-R transactivated by Ca2+-dependent tyrosine kinase, and that Ang II-induced fibronectin mRNA expression is regulated by two different mechanisms; transcriptional control by binding of c-fos/c-jun complex to the AP-1 site, and post-transcriptional control by mRNA stabilization due to autocrine and/or paracrine effects of TGF- β. Thus, this study suggested that the action of Ang II on extracellular matrix formation should be interpreted in association with the EGF-R signaling cascade. (Mol Cell Biochem 212: 187–201, 2000) More... »

PAGES

187-201

Book

TITLE

Control of Gene Expression by Catecholamines and the Renin-Angiotensin System

ISBN

978-1-4613-6955-4
978-1-4615-4351-0

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4615-4351-0_22

DOI

http://dx.doi.org/10.1007/978-1-4615-4351-0_22

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041337027


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