Open AccessbFGF attenuates endoplasmic reticulum stress and mitochondrial injury on myocardial ischaemia/reperfusion via activation of PI 3K/Akt/ ERK 1/2 pathway
Author(s) -
Wang Zhouguang,
Wang Yue,
Ye Junming,
Lu Xianghong,
Cheng Yi,
Xiang Lijun,
Chen Li,
Feng Wenke,
Shi Hongxue,
Yu Xichong,
Lin Li,
Zhang Hongyu,
Xiao Jian,
Li Xiaokun
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12346
Subject(s) - protein kinase b , pi3k/akt/mtor pathway , endoplasmic reticulum , ly294002 , mapk/erk pathway , oxidative stress , cardioprotection , reperfusion injury , microbiology and biotechnology , chemistry , unfolded protein response , pharmacology , mitochondrion , signal transduction , medicine , ischemia , biology , biochemistry
Extensive research focused on finding effective strategies to prevent or improve recovery from myocardial ischaemia/reperfusion (I/R) injury. Basic fibroblast growth factor (b FGF ) has been shown to have therapeutic potential in some heart disorders, including ischaemic injury. In this study, we demonstrate that b FGF administration can inhibit the endoplasmic reticulum ( ER ) stress and mitochondrial dysfunction induced in the heart in a mouse model of I/R injury. In vitro , b FGF exerts a protective effect by inhibiting the ER stress response and mitochondrial dysfunction proteins that are induced by tert‐Butyl hydroperoxide ( TBHP ) treatment. Both of these in vivo and in vitro effects are related to the activation of two downstream signalling pathways, PI3K/Akt and ERK 1/2. Inhibition of these PI3K/Akt and ERK 1/2 pathways by specific inhibitors, LY294002 and PD98059, partially reduces the protective effect of b FGF . Taken together, our results indicate that the cardioprotective role of b FGF involves the suppression of ER stress and mitochondrial dysfunction in ischaemic oxidative damage models and oxidative stress‐induced H9C2 cell injury; furthermore, these effects underlie the activation of the PI3K/Akt and ERK 1/2 signalling pathways.