Expression of AKR1C3 Protein in Human Keloid Skin Tissue

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.

Reactive Carbonyl Species as Potential Pro-Oxidant Factors Involved in Lichen Planus Pathogenesis

“…In our study, the levels of TAS were significantly lower in LP patients than in controls. These results could be explained by the ability of RCSs to regulate cell signaling pathways, cell proliferation, and the adaptation to stress [2,29,60]. The adaptation of cells to increased levels of RCSs in vivo, including 4-HNE and MDA, and the antioxidant cell protection are achieved by the regulation of several oxidative stress-related transcriptional factors (NRF2, AP-1, NF-Kb, and peroxisome proliferator-activated receptor - PPAR), coupled with the activation of stress response pathways (mitogen-activated protein kinase - MAPK, epidermal growth factor receptor - EGFR / Akt, protein kinase C - PKC) [1,61].…”

“…The resulting macromolecules may present structural alterations and changes of their physico-chemical effects (dysfunction or inactivation). To prevent tissue damage, RCSs are metabolized by several oxidoreductases, including aldo-ketoreductase (AKR), aldehyde-dehydrogenase (ADH), alcohol-dehydrogenase (ALDH), and glutathione-S-transferase (GST) [28,29]. In a previous study, we have demonstrated that an alteration in antioxidant defense systems may be involved in the pathogenesis of LP [30].…”