Journal
JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION
Volume 59, Issue 3, Pages 174-181Publisher
JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION
DOI: 10.3164/jcbn.16-26
Keywords
extracellular-superoxide dismutase; incretin-based therapy; exendin-4; epigenetics; diabetic retinopathy
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Funding
- JSPS KAKENHI [25460654]
- Gifu Pharmaceutical University
- Gifu University
- Grants-in-Aid for Scientific Research [25460654] Funding Source: KAKEN
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Extracellular-superoxide dismutase (genetic name SOD3) is a secreted anti-oxidative enzyme, and its presence in vascular walls may play an important role in protecting the vascular system against oxidative stress. Oxidative stress has been implicated in the pathogenesis of diabetic retinopathy; therefore, increases in extracellular-superoxide dismutase have been suggested to inhibit the progression of diabetic retinopathy. Incretin-based drugs such as glucagon-like peptide-1 receptor agonists are used in the treatment of type 2 diabetes. Glucagon-like peptide-1 receptor agonists are expected to function as extrapancreatic agents because the glucagon-like peptide-1 receptor is expressed not only in pancreatic tissues, but also in many other tissue types. We herein demonstrated that exendin-4, a glucagon-like peptide-1 receptor agonist, induced the expression of extracellular-superoxide dismutase in human retinal microvascular endothelial cells through epigenetic regulation. The results of the present study demonstrated that exendin-4 induced the expression of extracellularsuperoxide dismutase through histone H3 acetylation at the SOD3 proximal promoter region. Moreover, plasma extracellularsuperoxide dismutase concentrations in diabetic patients were elevated by incretin-based therapies. Therefore, incretin-based therapies may exert direct extrapancreatic effects in order to protect blood vessels by enhancing anti-oxidative activity.
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