Chemerin/ChemR23 axis triggers an inflammatory response in keratinocytes through ROS ‐sirt1‐NF‐κB signaling

In conclusion, chemerin can seduce inflammatory response and promote nuclear factor ‐κB (NF‐κB) activation through inhibition of sirtuin 1 (sirt1) activity by reactive oxygen species (ROS) production AbstractPsoriasis is a chronic disease which carries the emotional and social burden, promotes joint disability and raises comorbidity possibility in patients. Obesity is closely correlated with the occurrence of psoriasis and adipokines produced by adipose tissues were found to be critical culprits. Chemerin is one of them and its expression was increased in patients with psoriatic arthritis. In our hypothesis, chemerin might act on keratinocytes and promote an inflammatory response, which plays an essential role in psoriatic epidermis. To validate our hypothesis, HaCaT cells and primary human keratinocytes were treated with chemerin (5, 10, and 20  ng/mL for 24 hours). Enzyme‐linked immunosorbent assay (ELISA) was used to determine the secretion of inflammatory factors. Nuclear factor‐κB (NF‐κB) activation and p65 acetylation were evaluated by Western blot analysis. The expression and activity of sirtuin 1 (sirt1), a deacetylase a ct on p65, were also analyzed. The results showed that chemerin prompted inflammatory factors secretion, NF‐κB activation and p65 acetylation through chemerin receptor 23 receptor. Chemerin constrained the expression and deacetylase activity of sirt1 through augment of reactive oxygen species (RO S) production. Additionally, cheme...
Source: Journal of Cellular Biochemistry - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research