Fas/FasL expression in the hippocampus of neonatal rat brains follwing hypoxic-ischemic injury.
10.3345/kjp.2006.49.2.198
- Author:
Young Pyo CHANG
1
;
Myeung Ju KIM
;
Young Il LEE
;
Ik Je IM
;
Jae Ju CHO
;
Jong Wan KIM
;
Sung Moon YEO
Author Information
1. Department of Pediatrics, College of Medicine, Dankook University, Cheonan, Korea. ychang@dankook.ac.kr
- Publication Type:Original Article
- Keywords:
Fas;
Fas ligand;
Newborn;
Brain;
Hypoxia;
Ischemia
- MeSH:
Animals;
Anoxia;
Blotting, Western;
Brain*;
Carotid Artery, Common;
Fas Ligand Protein;
Hippocampus*;
Humans;
Infant, Newborn;
Ischemia;
Ligation;
Neurons;
Oxygen;
Rats*
- From:Korean Journal of Pediatrics
2006;49(2):198-202
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Fas is a cell surface receptor that transduces apoptotic death signals. Interaction of extracelluar domain of Fas with Fas ligand(FasL) triggers the apoptotic process in many diseases. We investigated the expression of Fas and FasL in the hippocampus of 7-day-old newborn rat brains following hypoxia-ischemia injury. METHODS: The 7-days-old newborn rats were exposed to 8 percent oxygen for two hours after the ligation of right common carotid arteries. The newborn rats were killed and their brains were removed at 12, 14 and 48 hours after hypoxic-ischemic injury. The expressions of Fas and FasL of the right hippocampus were observed by western blotting and immunofluorescent staining. RESULTS: Fas and FasL were strongly expressed in the right hippocampus ipsilateral to the ligation of the common carotid artery by western blotting at 12 hours following hypoxic-ischemic injury, and then slowly decreased. The immunofluorescent expressions of Fas and FasL strongly increased in the CA1 area of the right hippocampus at 12 and 24 hours following hypoxic-ischemic injury. The immunofluorescent expression of Fas decreased at 48 hours, but the expression of FasL persisted strongly at 48 hours following hypoxic-ischemic injury. CONCLUSION: The interaction of Fas with FasL on the cell surface may be involved in neuronal injury following hypoxic-ischemic injury in the developing brain.
