Open AccessAlterations in the expression of the apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE/ref-1) and DNA damage in the caudal region of acute and chronic spinal cord injured rats treated by embryonic neural stem cells
Author(s) -
Taner Dağcı,
Güliz Armağan,
Sibel Konyalıoğlu,
Ayfer Yalçın
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931388
Subject(s) - spinal cord , dna damage , spinal cord injury , medicine , oxidative stress , dna (apurinic or apyrimidinic site) lyase , lesion , ap site , pathology , biology , endocrinology , neuroscience , dna , genetics
The oxidative mechanisms of injury-induced damage of neuronswithin the spinal cord are not very well understood. We used amodel of T8-T9 spinal cord injury (SCI) in the rat to induceneuronal degeneration. In this spinal cord injury model, unilateralavulsion of the spinal cord causes oxidative stress of neurons. Wetested the hypothesis that apurinic/apyrimidinic endonuclease (orredox effector factor-1, APE/Ref-1) regulates this neuronaloxidation mechanism in the spinal cord region caudal to thelesion, and that DNA damage is an early upstream signal. Theembryonic neural stem cell therapy significantly decreased DNAdamage levels in both study groups – acutely (followed up to7 days after SCI), and chronically (followed up to 28 days afterSCI) injured animals. Meanwhile, mRNA levels of APE/Ref-1significantly increased after embryonic neural stem cell therapy inacutely and chronically injured animals when compared to acuteand chronic sham groups. Our data has demonstrated that anincrease of APE/Ref-1 mRNA levels in the caudal region of spinalcord strongly correlated with DNA damage after traumatic spinalcord injury. We suggest that DNA damage can be observed bothin lesional and caudal regions of the acutely and chronicallyinjured groups, but DNA damage is reduced with embryonicneural stem cell therapy.