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The adenoviral vector-mediated increase in apurinic/apyrimidinic endonuclease inhibits the induction of neuronal cell death after transient ischemic stroke in mice

Authors
 Hyun-Woo Kim  ;  Kyoung-Joo Cho  ;  Soo-Chul Park  ;  Hyun-Jeong Kim  ;  Gyung W. Kim 
Citation
 BRAIN RESEARCH, Vol.1274 : 1-10, 2009 
Journal Title
 BRAIN RESEARCH 
ISSN
 0006-8993 
Issue Date
2009
MeSH
Adenoviridae/genetics ; Animals ; Blotting, Western ; Cell Death/genetics ; Cerebrovascular Circulation/physiology ; DNA Fragmentation* ; DNA-(Apurinic or Apyrimidinic Site) Lyase/genetics* ; DNA-(Apurinic or Apyrimidinic Site) Lyase/metabolism ; Fluorescent Antibody Technique ; Free Radicals/metabolism ; Genetic Therapy/methods* ; Genetic Vectors ; In Situ Nick-End Labeling ; Infarction, Middle Cerebral Artery/complications ; Ischemic Attack, Transient/etiology ; Ischemic Attack, Transient/genetics* ; Ischemic Attack, Transient/pathology ; Laser-Doppler Flowmetry ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/pathology* ; Oxidative Stress/physiology ; Reperfusion Injury/etiology ; Reperfusion Injury/genetics* ; Reperfusion Injury/pathology
Keywords
DNA repair ; DNA fragmentation ; Cerebral ischemia ; Adenoviral vector
Abstract
Despite the correlation between changes in the levels of apurinic/apyrimidinic endonuclease and ischemic neuronal damage, no studies have addressed the question of whether increased APE/Ref-1 can prevent ischemic neuronal cell death in vivo. Using an adenoviral vector, we investigated whether increased APE/Ref-1 can inhibit the loss of APE/Ref-1 and thereby prevent oxidative DNA damage after transient focal cerebral ischemia. Mice were subjected to intraluminal suture occlusion of the middle cerebral artery for 1 h, followed by reperfusion. Pre-ischemic treatment of the adenoviral vector was introduced intracerebrally. An adenoviral vector harboring the entire APE/Ref-1 gene sequence or a control virus without the APE/Ref-1 sequence was introduced 3 days before ischemia/reperfusion (I/R). The reduction of APE/Ref-1 occurred before DNA fragmentation, which was shown by temporal and spatial analysis. Increased APE/Ref-1 significantly decreased DNA damage and infarct volume after I/R. In conclusion, increased APE/Ref-1 enhanced DNA repair and inhibited the induction of ischemic oxidative DNA damage and cerebral infarction after I/R
Full Text
http://www.sciencedirect.com/science/article/pii/S0006899309007355
DOI
10.1016/j.brainres.2009.04.006
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Gyung Whan(김경환) ORCID logo https://orcid.org/0000-0001-7053-4372
Kim, Hyun Woo(김현우)
Kim, Hyun Jeong(김현정)
Park, Soo Chul(박수철)
Cho, Kyuong Joo(조경주)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/104055
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