Open AccessFGF ‐2 suppresses expression of nephronectin via JNK and PI 3K pathways
Author(s) -
Kato Tadashi,
Yamada Atsushi,
Ikehata Mikiko,
Yoshida Yuko,
Sasa Kiyohito,
Morimura Naoko,
Sakashita Akiko,
Iijima Takehiko,
Chikazu Daichi,
Ogata Hiroaki,
Kamijo Ryutaro
Publication year - 2018
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12421
Subject(s) - oncostatin m , fibroblast growth factor , microbiology and biotechnology , pi3k/akt/mtor pathway , chemistry , signal transduction , growth factor , extracellular matrix , kinase , biology , cytokine , receptor , biochemistry , interleukin 6 , immunology
Nephronectin (Npnt), an extracellular matrix protein, is a ligand for integrin α8β1 and is involved in the development of various organs, such as the kidneys, bones, liver, and muscles. Previously, we found that Npnt expression was inhibited by various cytokines including transforming growth factor‐β ( Tgf ‐β) and oncostatin M (Osm). Fibroblast growth factor ( Fgf )‐2, otherwise known as basic Fgf, also plays important roles in skeletal development and postnatal osteogenesis. In this study, Npnt expression was found to be suppressed by Fgf ‐2 in MC 3T3‐E1 cells, an osteoblast‐like cell line, in a dose‐ and time‐dependent manners. Furthermore, Fgf ‐2‐mediated Npnt mRNA suppression was shown to involve the Jun N‐terminal kinase ( JNK ) and phosphoinositide‐3 kinase ( PI 3K) pathways. Together, our results suggest that FGF ‐2 suppresses Npnt gene expression via JNK and PI 3K pathways.