Arch Aesthetic Plast Surg.  2016 Feb;22(1):35-39. 10.14730/aaps.2016.22.1.35.

Expression of AKR1C3 Protein in Human Keloid Skin Tissue

• Nam DH
• Lee D
• Kim CH
• Kang SG
• Shin HS
• Lee YM

• KMID: 2155845
• DOI: http://doi.org/10.14730/aaps.2016.22.1.35

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.

Keyword

Keloid; Reactive oxygen species; Skin

MeSH Terms

Blotting, Western
Connective Tissue
Down-Regulation
Humans*
Keloid*
Metabolism
Oxidative Stress
Oxidoreductases
Reactive Oxygen Species
Skin*
Wounds and Injuries
Oxidoreductases
Reactive Oxygen Species