Expression of B/K protein in the hippocampus of kainate-induced rat seizure model.
B/K protein is a newly identified member of double C2-like domain protein family. We examined the expression of B/K protein in the hippocampus of kainate-induced rat seizure model. Intraperitoneal injection of kainate increased the immunoreactivity to B/K protein in the CA1 to CA3 of the hippocampus. B/K protein expression began to increase at 6 h, reached the maximum at 12 h, and then returned nearly to the normal level at 72 h after the injection of kainate (12 mg/kg), and it was also dependent on the dose of kainate between 4 and 16 mg/kg. In electron microscopic and subcellular fractionation studies, B/K protein was localized in the endoplasmic reticulum (ER) of the hippocampus. Kainate also induced the expression of BiP, a typical ER stress marker protein, in the hippocampus and the cortex, and it was coexpressed with B/K protein. Moreover, thapsigargin-induced ER stress caused upregulation of B/K protein expression in PC12 cells. In conclusion, our data showing the induction of both B/K protein expression and ER stress response in the hippocampus of kainate seizure model, and ER-specific expression and ER stress-induced expression of B/K strongly suggest the possible role of B/K protein in epileptogenesis or epilepsy-induced neuronal damage.
Jang
Yoon-Seong
YS
Department of Biochemistry, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, South Korea.
Lee
Mun-Yong
MY
Choi
Sung-Ho
SH
Kim
Mi-Young
MY
Chin
Hemin
H
Jeong
Seong-Whan
SW
Kim
In-Kyung
IK
Kwon
Oh-Joo
OJ
D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D000091342:Endoplasmic Reticulum Chaperone BiP; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004827:Epilepsy / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D018690:Excitatory Amino Acid Agonists; D006360:Heat-Shock Proteins; D006624:Hippocampus / Q000378:metabolism* / Q000503:physiopathology / Q000648:ultrastructure; D007150:Immunohistochemistry; D007608:Kainic Acid; D008297:Male; D008854:Microscopy, Electron; D018832:Molecular Chaperones / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D016716:PC12 Cells; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D013312:Stress, Physiological / Q000378:metabolism / Q000503:physiopathology; D050857:Synaptotagmins; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
D002352:Carrier Proteins; D000091342:Endoplasmic Reticulum Chaperone BiP; D004791:Enzyme Inhibitors; D018690:Excitatory Amino Acid Agonists; D006360:Heat-Shock Proteins; D018832:Molecular Chaperones; D009419:Nerve Tissue Proteins; C409229:Syt17 protein, rat; D050857:Synaptotagmins; D007608:Kainic Acid