Open AccessFGF 1 improves functional recovery through inducing PRDX 1 to regulate autophagy and anti‐ROS after spinal cord injury
Author(s) -
Li Jiawei,
Wang Qingqing,
Cai Hanxiao,
He Zili,
Wang Haoli,
Chen Jian,
Zheng Zengming,
Yin Jiayu,
Liao Zhiyong,
Xu Huazi,
Xiao Jian,
Gong Fanghua
Publication year - 2018
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.13566
Subject(s) - spinal cord injury , autophagy , neuroprotection , spinal cord , fibroblast growth factor , in vivo , microbiology and biotechnology , regeneration (biology) , chemistry , pharmacology , biology , neuroscience , apoptosis , biochemistry , receptor
Fibroblast growth factor 1 ( FGF 1) is thought to exert protective and regenerative effects on neurons following spinal cord injury ( SCI ), although the mechanism of these effects is not well understood. The use of FGF 1 as a therapeutic agent is limited by its lack of physicochemical stability and its limited capacity to cross the blood‐spinal cord barrier. Here, we demonstrated that overexpression of FGF 1 in spinal cord following SCI significantly reduced tissue loss, protected neurons in the ventricornu, ameliorated pathological morphology of the lesion, dramatically improved tissue recovery via neuroprotection, and promoted axonal regeneration and remyelination both in vivo and in vivo. In addition, the autophagy and the expression levels of PRDX 1 (an antioxidant protein) were induced by AAV ‐ FGF 1 in PC 12 cells after H 2 O 2 treatment. Furthermore, the autophagy levels were not changed in PRDX 1‐suppressing cells that were treated by AAV ‐ FGF 1. Taken together, these results suggest that FGF 1 improves functional recovery mainly through inducing PRDX 1 expression to increase autophagy and anti‐ ROS activity after SCI .