Expression of AKR1C3 Protein in Human Keloid Skin Tissue.
10.14730/aaps.2016.22.1.35
- Author:
Doo Hyun NAM
1
;
Dawoon LEE
;
Chul Han KIM
;
Sang Gue KANG
;
Ho Seong SHIN
;
Young Man LEE
Author Information
1. Department of Plastic and Reconstructive Surgery, Soonchunhyang University College of Medicine, Cheonan, Korea. youngman@schmc.ac.kr
- Publication Type:Original Article
- Keywords:
Keloid;
Reactive oxygen species;
Skin
- MeSH:
Blotting, Western;
Connective Tissue;
Down-Regulation;
Humans*;
Keloid*;
Metabolism;
Oxidative Stress;
Oxidoreductases;
Reactive Oxygen Species;
Skin*;
Wounds and Injuries
- From:Archives of Aesthetic Plastic Surgery
2016;22(1):35-39
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
