Decreased Expression of Type 5 17 beta-Hydroxysteroid Dehydrogenase (AKR1C3) Protein Identified in Human Diabetic Skin Tissue
- Authors
- Cho, Moon-Kyun
- Issue Date
- Nov-2013
- Publisher
- 대한피부과학회
- Keywords
- AKR1C3; Diabetic skin; Type 5 17 beta-hydroxysteroid dehydrogenase
- Citation
- Annals of Dermatology, v.25, no.4, pp 423 - 427
- Pages
- 5
- Journal Title
- Annals of Dermatology
- Volume
- 25
- Number
- 4
- Start Page
- 423
- End Page
- 427
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/13250
- DOI
- 10.5021/ad.2013.25.4.423
- ISSN
- 1013-9087
2005-3894
- Abstract
- Background: Diabetes is characterized by chronic hyperglycemia, and hyperglycemia can increase reactive oxygen species (ROS) production from the mitochondrial electron transport chain. The formation of ROS in cells induces oxidative stress and activates oxidative damage-inducing genes. There is no research on the protein levels of oxidative damage-related genes AKR1C3 in human diabetic skin. We explored the expression of AKR1C3 in diabetic skin compared with normal skin tissue. Objective: To compare the expression of AKR1C3 in normal skin versus diabetic skin. Methods: AKR1C3 expression was evaluated by western blotting in 6 diabetic skin tissue samples and 6 normal skin samples. Immunohistochemical staining was carried out to analyze AKR1C3 expression in the 6 diabetic skin tissue samples (July 2009 to December 2011; Department of Plastic and Reconstructive Surgery at Soonchunhyang University Seoul Hospital, Seoul, Korea). Results: The western blotting showed a significant reduction in AKR1C3 protein expression in diabetic skin tissue compared to normal tissue. Immunohistochemical examination of AKR1C3 showed that it was weakly expressed in all diabetic skin samples. Conclusion: We believe that AKR1C3 is related to diabetic skin in altered metabolic states which elevate ROS production.
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