Division of Plastic Surgery, Department of Surgery, Chi Mei Medical Center, Tainan, Taiwan, Republic of China.
Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan, Republic of China.
Exp Dermatol. 2017 Sep;26(9):832-835. doi: 10.1111/exd.13292. Epub 2017 Apr 11.
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.
在这项研究中，我们研究了在生理浓度的 Ca（1.8mM）下，紫外线 B（UVB）辐射与表皮生长因子（EGF）共同作用对角质细胞分化的调节作用。此外，许多研究中用于测量信号转导和激酶磷酸化的生长因子剥夺在生理上是不现实的。因此，所有实验中还包含了 1%的血清。我们发现，UVB 辐射依赖于 Ca 诱导形态分化，并增加角蛋白 1 和 10（K1/K10）的表达。EGF 的处理抑制了这两种物质的表达。在静止细胞中，急性 EGF 处理刺激 ERK 的磷酸化，而在慢性 EGF 处理或 1%血清暴露下，ERK 迅速脱敏。UVB 辐射诱导的角质细胞分化需要 TRPV1 介导的 Ca 内流。Ca 依赖性 ERK 磷酸化负责 K1/10 的表达。在 UVB 辐射期间用 EGF 共同处理细胞，通过使 ERK 磷酸化脱敏来抑制 UVB 辐射诱导的分化。
