Highlights
- •Bif-1 improves OGD/R-induced cortical neurons survival and autophagy.
- •Bif-1 inhibits OGD/R-induced cell apoptosis and the activity of caspase-3.
- •Cell autophagy inhibitor 3-MA suppresses OGD/R-induced cortical neurons survival.
- •Inhibition Bif-1 promotes OGD/R-induced cell autophagy in cortical neurons.
- •ERK1/2 pathway is involved in the effects of Bif-1 on OGD/R-induced cell survival.
Abstract
Bax interacting factor-1 (Bif-1), a multifunctional protein, can regulate cell apoptosis
and autophagy. Up-regulation of Bif-1 expression has been associated with neuronal
survival. Moreover, several studies have reported that Bif-1 is involved in ischemic
stroke. However, the specific function of Bif-1 in cerebral ischemia-reperfusion (I/R)
injury is not well understood. The aim of this study is to expose the potential protective
effect of Bif-1 against cerebral I/R injury and its related mechanism. In the current
study, we showed that adenovirus-mediated Bif-1-overexpression promoted oxygen and
glucose deprivation followed by reperfusion (OGD/R)-treated cortical neurons' survival
and reduced the cell apoptotic rate. We found that caspase-3 activity was inhibited
by Bif-1 overexpression. In addition, we observed that Bif-1 overexpression induces
cell autophagy, and the autophagy-specific inhibitor 3-Methyladenine (3-MA) attenuates
cell survival. Interestingly, knockdown of Bif-1 resulted in attenuation of neuron
survival, promotion of cell apoptosis and suppression of cell autophagy in neurons.
In addition, knockdown of Bif-1 inhibited ERK1/2 activation. Our observations implicated
Bif-1 as a novel target of cerebral I/R injury and played a neuroprotective effect
via promoting cell survival and reducing apoptosis.
Abbreviations:
Bif-1 (Bax interacting factor-1), 3-MA (3-Methyladenine), OGD/R (oxygen and glucose deprivation followed by reperfusion), MTT (3-(4,5-dimethylthi-azol-2-yl)-2,5-diphenyl-tetrazolium bromide), ECL (enhanced chemiluminescence)Keywords
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Article info
Publication history
Published online: July 20, 2015
Accepted:
July 17,
2015
Received in revised form:
June 23,
2015
Received:
February 12,
2015
Footnotes
☆Conflicts of interest: None.
Identification
Copyright
© 2015 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
