Hyperglycemia exacerbates downregulation of dynamin-like protein 1 in ischemic cerebral injury.
10.5625/lar.2017.33.3.202
- Author:
Dong Ju PARK
1
;
Myeong Ok KIM
;
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:Original Article
- Keywords:
Brain ischemia;
hyperglycemia;
MCAO;
dynamin-like protein 1
- MeSH:
Adult;
Animals;
Blotting, Western;
Brain;
Brain Injuries;
Brain Ischemia;
Cerebral Cortex;
Down-Regulation*;
Humans;
Hyperglycemia*;
Infarction, Middle Cerebral Artery;
Male;
Mitochondrial Dynamics;
Models, Animal;
Neurodegenerative Diseases;
Polymerase Chain Reaction;
Proteomics;
Rats;
Streptozocin;
Stroke
- From:Laboratory Animal Research
2017;33(3):202-208
- CountryRepublic of Korea
- Language:English
-
Abstract:
Ischemic stroke is one of the leading causes of adult disability and death. Hyperglycemia is associated with an increased risk of stroke and poor outcomes after brain injury. Dynamin-like protein I (DLP-1) regulates mitochondrial fission and promotes mitochondrial dynamics. Neurodegenerative diseases are associated with mitochondrial dysfunction, and the downregulation of DLP-1 has been previously identified in a stroke animal model. Here, we investigated the changes in DLP-1 protein expression in an animal model of focal cerebral ischemia with induced hyperglycemia. Streptozotocin (40 mg/kg) was intraperitoneally injected into male rats to induce hyperglycemia, and middle cerebral artery occlusion (MCAO) was surgically induced 4 weeks after streptozotocin treatment. Brain tissue was isolated 24 hours after MCAO, and cerebral cortex samples were used for this study. Proteomics revealed a decrease in DLP-1 expression in MCAO animals when compared with controls, and this downregulation was more prominent in MCAO animals with hyperglycemia. Reverse-transcription polymerase chain reaction and Western blot analyses confirmed that DLP-1 was significantly downregulated in MCAO-injured animals with hyperglycemia compared to those without hyperglycemia. The decrease in DLP-1 indicates mitochondrial morphological changes and dysfunction. Together, these results suggest that the severe decrease of DLP-1 seen after brain injury under hyperglycemic conditions may exacerbate the damage to the brain.
