Premium
Neuroprotection of brain‐derived neurotrophic factor against hypoxic injury in vitro requires activation of extracellular signal‐regulated kinase and phosphatidylinositol 3‐kinase
Author(s) -
Sun Xiaomei,
Zhou Hui,
Luo Xiaoli,
Li Shengfu,
Yu Dan,
Hua Jiping,
Mu Dezhi,
Mao Meng
Publication year - 2008
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2007.11.005
Subject(s) - creb , mapk/erk pathway , neuroprotection , neurotrophic factors , microbiology and biotechnology , kinase , protein kinase a , brain derived neurotrophic factor , p38 mitogen activated protein kinases , signal transduction , tropomyosin receptor kinase b , biology , neuroscience , chemistry , transcription factor , biochemistry , receptor , gene
Intrauterine asphyxia is one of the major contributors for perinatal death, mental and physical disorders of surviving children. Brain‐derived neurotrophic factor (BDNF) provides a promising solution to hypoxic injury due to its survival‐promoting effects. In an attempt to identify possible molecular mechanisms underlying the neuroprotective role of BDNF, we studied extracellular signal‐regulated kinase (ERK), phosphatidylinositol 3‐kinase (PI‐3‐K) and p38 mitogen‐activated protein kinase (MAPK) pathways. We demonstrated that BDNF protected cortical neurons against hypoxic injury in vitro via activation of both the ERK and PI‐3‐K pathways but not the p38 MAPK pathway. We also showed that both hypoxic stimuli and exogenous BDNF treatment phosphorylated the cyclic AMP response element‐binding protein (CREB) and that CREB phosphorylation induced by BDNF was mediated via the ERK pathway in cultured cortical neurons.