Abstract
Endoplasmic reticulum (ER) stress may play a role in status epilepticus (SE). Sprague–Dawley rats were randomized into three groups: control (saline), SE (pentylenetetrazol), and dentate gyrus (DG), pretreated with 2-deoxy-d-glucose (2-DG). Expression levels of glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), eukaryotic initiation factor 2α (eIF2α), and protein kinase RNA-like ER kinase (PERK) were determined. CHOP messenger RNA (mRNA) and protein expression levels in SE group were significantly increased as compared to the control group (P < 0.0001), and significantly decreased in DG group as compared to the SE group (P < 0.0001). Phosphorylated eIF-2α protein expression level in SE group was significantly increased as compared to the control group (P < 0.0001) and significantly decreased in DG group as compared to the SE group (P < 0.0001). GRP messenger RNA expression levels and protein levels in SE group was significantly increased as compared to the control group (P < 0.0001) and significantly decreased in DG group as compared to the SE group (P < 0.0001). Phosphorylated PERK protein expression level in SE group was significantly increased as compared to the control group (P < 0.0001), and significantly decreased in DG group as compared to the SE group (P < 0.0001) at the time of 12 and 24 h. Our results suggest that brain injury from SE might involve ER stress via the pro-apoptotic PERK–eIF2α–CHOP signaling pathway.
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This study was supported by Key Project supported by Medical Science and Technology Development Foundation, Nanjing Department of Health (ZKX10024).
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Chen, J., Zheng, G., Guo, H. et al. Role of Endoplasmic Reticulum Stress via the PERK Signaling Pathway in Brain Injury from Status Epilepticus. J Mol Neurosci 53, 677–683 (2014). https://doi.org/10.1007/s12031-014-0236-4
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DOI: https://doi.org/10.1007/s12031-014-0236-4