ABSTRACT
We previously reported that epidermal glycation causes an increase in saturated fatty acid (FA) content in a differentiated reconstructed skin model and HaCaT cells. However, the relationship between ceramides (CERs) and glycation and their effects on stratum corneum (SC) barrier function was not elucidated. In this study, we investigated the effect of glycation on lipid content in 6-day-old cultured reconstructed skin. We used the EPISKIN RHE 6D model and induced glycation using glyoxal. In addition to transepidermal water loss, content of CERs, cholesterol and FA in the reconstructed epidermal model were analyzed by high performance thin layer chromatography. Expression of genes related to ceramide metabolism was determined by real time RT-PCR. Membrane fluidity of stratum corneum lipid liposomes (SCLL) that mimic glycated epidermis was analyzed using an electron spin resonance technique. It was found that FA was significantly increased by glycation. CER[NS], [AP], and cholesterol were decreased in glycated epidermis. Expression of ceramide synthase 3 (CERS3) was significantly decreased while fatty acid elongase 3 was increased by glyoxal in a dose dependent manner. Membrane fluidity of SCLL mimicking the lipid composition of glycated epidermis was increased compared with controls. Therefore, disruption of CER and FA content in glycated epidermis may be regulated via CERS3 expression and contribute to abnormal membrane fluidity.
Abbreviations
AD | = | Atopic dermatitis |
AGE | = | Advanced glycation end products |
CER | = | Ceramide |
Chol | = | Cholesterol |
5-DSA | = | 5-DOXYL stearic acid |
ESR | = | Electron skin resonance |
FA | = | Fatty acids |
GO | = | Glyoxal |
SCLL | = | Stratum corneum lipid liposome |
TEWL | = | Transepidermal water loss |
Disclosure of potential conflicts of interest
No potential conflicts of interest were disclosed.
Acknowledgments
The author gratefully acknowledges the technical assistance of Ms. Yuki Sagawa.