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Oxygen‐glucose deprivation preconditioning protects neurons against oxygen‐glucose deprivation/reperfusion induced injury via bone morphogenetic protein‐7 mediated ERK , p38 and Smad signalling pathways
Author(s) -
Guan Junhong,
Du Shaonan,
Lv Tao,
Qu Shengtao,
Fu Qiang,
Yuan Ye
Publication year - 2016
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12492
Subject(s) - smad , p38 mitogen activated protein kinases , mapk/erk pathway , microbiology and biotechnology , oxygen , chemistry , bone morphogenetic protein , reactive oxygen species , bone morphogenetic protein 2 , signal transduction , biochemistry , biology , gene , in vitro , organic chemistry
Summary Bone morphogenetic protein ( BMP )‐7 mediated neuroprotective effect of cerebral ischemic preconditioning ( IPC ) has been studied in an ischemic animal model, but the underlying cellular mechanisms have not been clearly clarified. In this study, primary cortical neurons and the SH ‐ SY 5Y cell line were used to investigate the role of BMP ‐7 and its downstream signals in the neuroprotective effects of oxygen‐glucose deprivation preconditioning ( OGDPC ). Immunocytochemistry was used to detect the expression of neurofilament in neurons. MTT and lactate dehydrogenase activity assays were used to measure the cytotoxicity. Western blot was used to detect the protein expression of BMP ‐7 and downstream signals. BMP inhibitor, mitogen‐activated protein kinase inhibitors, Smad inhibitor and si RNA of Smad 1 were used to investigate the role of corresponding signalling pathways in the OGDPC . Results showed that OGDPC ‐induced overexpression of BMP ‐7 in primary cortical neurons and SH ‐ SY 5Y cells. Both of endogenous and exogenous BMP ‐7 could replicate the neuroprotective effects seen in OGDPC pretreatment. In addition, extracellular regulated protein kinases, p38 and Smad signalling pathway were found to be involved in the neuroprotective effects mediated by OGDPC via BMP ‐7. This study primarily reveals the cellular mechanisms of the neuroprotection mediated by OGDPC , and provides evidence for better understanding of this intrinsic factor against ischemia.