Expression of AKR1C3 Protein in Human Keloid Skin TissueExpression of AKR1C3 Protein in Human Keloid Skin Tissue
- Other Titles
- Expression of AKR1C3 Protein in Human Keloid Skin Tissue
- Authors
- 남두현; 이다운; 김철한; 강상규; 신호성; 이영만
- Issue Date
- 2016
- Publisher
- 대한미용성형외과학회
- Keywords
- Keloid; Reactive oxygen species; Skin
- Citation
- Archives of Aesthetic Plastic Surgery, v.22, no.1, pp 35 - 39
- Pages
- 5
- Journal Title
- Archives of Aesthetic Plastic Surgery
- Volume
- 22
- Number
- 1
- Start Page
- 35
- End Page
- 39
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/9888
- ISSN
- 2234-0831
2288-9337
- Abstract
- Keloids are abnormal wound responses that are caused by hyperproliferative growth of connective tissue during the healing process. Recent research findings introduced the roles of reactive oxygen species (ROS) in the process of keloid formation.
ROS induces oxidative stress and promotes the activities of oxidative damage-inducible genes. Aldo-keto reductase 1C3 (AKR1C3) prevents destructive ROS toxicity by detoxification of reactive carbonyl species. Thus, this study aimed to compare the expression of AKR1C3 in both normal and keloid skin in vivo.
Six specimens of normal skin and six specimens of keloid tissues from human subjects were used to evaluate the expression of AKR1C3 by immunofluorescent staining of tissues and western blotting.
By western blotting, it was confirmed that the amount of AKR1C3 protein is significantly reduced in keloid tissues compared to normal tissues. Weak expression of AKR1C3 was also found in keloid tissues by immunofluorescent staining.
This study confirmed that the expression of AKR1C3 protein participates in ROS metabolism and plays a part in the downregulation of human keloid formation. To the best of our knowledge, this is the first work that reveals that AKR1C3 can affect the formation of keloids.
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Collections - College of Medicine > Department of Plastic Surgery > 1. Journal Articles
- College of Medicine > Department of Plastic Surgery > 1. Journal Articles
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