Aging Skin and Comorbidities in Atopic dermatitis – Are Advanced Glycation End Products Guilty? : Dataset

Published: 4 February 2020| Version 1 | DOI: 10.17632/dstwbpd2rd.1
Contributors:
Haley Hong,
Min Jeong Kim,
Jun Ki Hong,
Hyun Ha Noh,
Kui Young Park,
Mi Kyung Lee,
Seong Jun Seo

Description

Advanced glycation end products (AGEs) interact with the membrane-bound receptor for AGEs (RAGE), consequently amplifying the inflammatory response. Soluble receptor for AGE (sRAGE) and endogenous secretory RAGE (esRAGE) act as decoys for AGE and competitively sequester RAGE ligands, thereby serving a cytoprotective role. Our objective was to investigate AGE expression and their receptors in the serum and skin of patients with atopic dermatitis (AD). In this case-control study, the levels of AGE, sRAGE, and esRAGE were measured in the blood samples and corneocytes of 29 adult patients with AD and 12 healthy controls by ELISA. Corneocyte AGE levels increased in the AD group (P = .002). Higher corneocyte AGE levels were observed in the severe AD than in the mild AD. No significant difference in serum AGE level was observed in patients with AD and healthy controls. Serum sRAGE markedly decreased in patients with AD (P = .007) and serum esRAGE followed a similar trend. In conclusion, dermal accumulation of AGE in AD may have a role in skin inflammation and aging. The potential after-effects of reduced neutralizer on systemic risk need further evaluation.

Files

Institutions

Chung-Ang University College of Medicine and Graduate School of Medicine

Categories

Biomarkers, Inflammation, Advanced Glycation End Product Receptor Affecting Agent, Aging, Atopic Dermatitis

License