Focal cerebral ischemic injury decreases calbindin expression in brain tissue and HT22 cells.
10.5625/lar.2013.29.3.156
- Author:
In Ohk OUH
1
;
Young Min KIM
;
Sang A GIM
;
Phil Ok KOH
Author Information
1. Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, Jinju, Korea. pokoh@gnu.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Glutamate;
middle cerebral artery occlusion;
calbindin
- MeSH:
Animals;
Blotting, Western;
Brain;
Brain Injuries;
Brain Ischemia;
Calcium;
Calcium-Binding Protein, Vitamin D-Dependent;
Carrier Proteins;
Cell Death;
Cell Line;
Cerebral Cortex;
Glutamic Acid;
Humans;
Infarction, Middle Cerebral Artery;
Male;
Neurons;
Rats
- From:Laboratory Animal Research
2013;29(3):156-161
- CountryRepublic of Korea
- Language:English
-
Abstract:
Calbindin is a calcium binding protein that controls intracellular calcium levels and has a neuroprotective function against apoptotic stimuli. We investigated the expression of calbindin in ischemic brain injury. Focal cerebral ischemia was induced in male rats by middle cerebral artery occlusion (MCAO) and cerebral cortices were collected 24 h after MCAO. Cerebral ischemia significantly increased infarct volume. RT-PCR and Western blot analyses showed that MCAO injury induced a decrease of calbindin expression. Moreover, immunohistochemical staining showed that the number of calbindin-positive cells decreased in ischemic regions of MCAO-operated animals. In cultured hippocampal-derived cell lines, glutamate exposure increased intracellular Ca2+ concentrations and decreased calbindin expression. Taken together, both in vivo and in vitro results demonstrated decreases of calbindin after neuronal cell injury. These results suggest that decreases of calbindin in ischemic brain injury contribute to neuronal cell death.
