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Hepatocyte Growth Factor Inhibits Lipopolysaccharide-Induced Oxidative Stress via Epithelial Growth Factor Receptor Degradation
Author(s) -
Kazutaka Shimizu,
Yoshiaki Taniyama,
Fumihiro Sanada,
Junya Azuma,
Masaaki Iwabayashi,
Kazuma Iekushi,
Hiromi Rakugi,
Ryuichi Morishita
Publication year - 2012
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.300041
Subject(s) - oxidative stress , hepatocyte , lipopolysaccharide , degradation (telecommunications) , microbiology and biotechnology , hepatocyte growth factor receptor , hepatocyte growth factor , chemistry , growth factor , receptor , endocrinology , medicine , biology , biochemistry , in vitro , c met , telecommunications , computer science
Lipopolysaccharide (LPS) triggers sepsis and systemic inflammatory response syndrome, which results in multiple organ failure. Our recent reports demonstrated that hepatocyte growth factor (HGF) attenuated angiotensin II-induced oxidative stress via epithelial growth factor receptor (EGFR) degradation in vascular smooth muscle cells. Here, we examined whether HGF can protect against systemic inflammatory response syndrome induced by LPS and investigated the mechanism.

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