Ultraviolet B irradiation increases keratin 1 and keratin 10 expressions in HaCaT keratinocytes via TRPV1 activation and ERK phosphorylation

Abstract

In this study, we characterized the effect of ultraviolet B (UVB) irradiation with or without epidermal growth factor (EGF) on the regulation of keratinocyte differentiation under physiological concentration of Ca (1.8 mM). In addition, growth factor deprivation used to measure signal transduction and kinase phosphorylation in many studies is physiologically unreal. Therefore, 1% of serum was also included in all experiment. We found that UVB irradiation Ca dependently induced morphological differentiation and increased keratin 1 and 10 (K1/K10) expressions. Both were inhibited by treatment of cells with EGF. In quiescent cells, phosphorylation of ERK was stimulated by acute EGF treatment, while it rapidly desensitized in chronic EGF treatment or 1% serum exposure. UVB irradiation-induced keratinocyte differentiation required Ca influx through TRPV1. Ca -dependent phosphorylation of ERK was responsible for the expression of K1/10. Cotreatment of cells with EGF during UVB irradiation inhibits the UVB irradiation-induced differentiation by desensitizing ERK phosphorylation.

Increased green autofluorescence is a marker for non-invasive prediction of H2O2-induced cell death and decreases in the intracellular ATP of HaCaT cells

“…Our previous study has indicated that UV, a factor that can induce oxidative stress, induces increased green AF of mouse skin by producing cysteine protease-mediated degradation of keratin 1 (9). Because HaCaT keratinocytes express keratin 1 (6,13), we propose that H 2 O 2 may induce increased green AF of the cells by producing alterations of keratin 1. Future studies are needed to test the validity of this proposal.…”

A new copper ionophore DPMQ protects cells against ultraviolet B irradiation by inhibiting the TRPV1 channel

“…As shown in the bottom traces in Figure b, bradykinin induced an increase in the intracellular Ca 2+ concentration and the amplitude of the increase was unaffected by the lack of extracellular Ca 2+ or the presence of capsazepine, DPMQ, DPMQ plus TTM, or disulfiram, thus ruling out the possibility that DPMQ acts as a Ca 2+ chelator and suggesting that it inhibits the TRPV1 channel. It has been shown that UVB irradiation activates the TRPV1 channel in HaCaT keratinocytes (Huang, Ma, Liu, Chen, & Chueh, ; Lee et al, ). We therefore examined whether DPMQ had an inhibitory effect on TRPV1 channel activation in HaCaT cells.…”

Weak Ultraviolet B Enhances the Mislocalization of Claudin-1 Mediated by Nitric Oxide and Peroxynitrite Production in Human Keratinocyte-Derived HaCaT Cells

“…These results suggest that TRPV1 is involved in the weak UVB-induced response in HaCaT cells. UVB irradiation increases keratin 1 and 10 expression mediated via activation of TRPV1 in HaCaT cells [ 37 ]. The expression of NOS3 was increased by UVB irradiation, which was inhibited by TRPV1 antagonists ( Figure 8 A).…”