Effect of Hypoxia Mimetic Cobalt Chloride on the Expression of Extracellular-Superoxide Dismutase in Retinal Pericytes
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概要
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The initial clinical stage of diabetic retinopathy (DR) is characterized by the development of intraretinal microvascular abnormalities. The increased formation of reactive oxygen species (ROS) is thought to be a key event in the pathogenesis of DR. Extracellular-superoxide dismutase (EC-SOD) is an anti-inflammatory enzyme that is distributed mainly in vascular cells and protects cells from ROS by scavenging superoxide anion. Treatment with cobalt chloride (CoCl2) decreased the expression of EC-SOD but not other SOD isozymes in pericytes accompanied with an increase of intracellular ROS production. Pre-treatment with N-acetylcysteine (NAC) significantly suppressed the ROS production and down-regulation of EC-SOD. We observed the activation of caspase-3 and DNA fragmentation as signs of apoptotic process by CoCl2 treatment. In addition, these phenomena were significantly inhibited by pre-treatment with NAC. EC-SOD enhancer 4-phenyl butyric acid also suppressed the caspase-3 activation. It is known that the presence of a high level of EC-SOD throughout the vessel walls might have an important protective role against superoxide in the vascular system. The decrease in EC-SOD expression accompanied with elevation of ROS level in pericytes under hypoxia might induce and/or promote the ROS-triggered apoptosis of pericytes and the development of pathogenesis in DR.
著者
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ADACHI Tetsuo
Laboratory of clinical Pharmaceutics, Gifu Pharmaceutical University
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Adachi Tetsuo
Laboratory Of Clinical Pharmaceutics Gifu Pharmaceutical University
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HARA Hirokazu
Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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Aida Kazunari
Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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Nishihara Hiroko
Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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Kamiya Tetsuro
Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University
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