Gu Wei-Jie, Ma Hui-Jun, Zhao Guang, Yuan Xiao-Ying, Zhang Ping, Liu Wen, Ma Li-Juan, Lei Xiao-Bing
Department of Dermatology, The General Hospital of Air Force, No. 30 Fucheng Road, Haidian District, Beijing, 100142, China.
Arch Dermatol Res. 2014 Aug;306(6):583-90. doi: 10.1007/s00403-014-1461-y. Epub 2014 Mar 27.
Heat is known as an environmental factor that causes significant skin pigmentation, but its effects on melanogenesis have been poorly studied. It has been shown that mitogen-activated protein kinase (MAPK) is involved in ultraviolet B (UVB) and stress-induced melanogenesis in melanocytes. In this study, we investigated the effects of heat and UVB, on melanocyte melanogenesis, differentiation, and MAPK phosphorylation. The results showed that heat (1 h at 40 °C for 5 days) increased cell dendrites, enlarged cell bodies, and induced extracellular signal-regulated kinases (ERK)/p38/MITF activation but did not influence melanogenesis of human epidermal melanocytes from skin phototype III. UVB irradiation (20 mJ/cm(2) for 5 days) induced melanogenesis and c-jun N-terminal kinases (JNK)/p38/MITF/tyrosinase activation in melanocytes from skin phototype III. UVB combined with heat resulted in much more significant tyrosinase activation and melanogenesis as compared with UVB alone in melanocytes from skin phototype III. Furthermore, heat treatment and UVB irradiation induced JNK, ERK, and p38 activation but not melanogenic and morphological changes in melanocytes from skin phototype I. These findings suggested that heat promoted melanocyte differentiation, probably via heat-induced ERK/p38/MITF/activation. Furthermore, heat had an additive effect on the UVB-induced tyrosinase activation and melanogenesis. These results provide a new clue for dermatologists for the treatment of hypopigmented skin disease with heat combined with UVB irradiation.
热被认为是一种导致显著皮肤色素沉着的环境因素,但其对黑素生成的影响尚未得到充分研究。有研究表明,丝裂原活化蛋白激酶(MAPK)参与黑素细胞中紫外线B(UVB)和应激诱导的黑素生成。在本研究中,我们调查了热和UVB对黑素细胞黑素生成、分化及MAPK磷酸化的影响。结果显示,热(40℃处理1小时,持续5天)增加了细胞树突、增大了细胞体,并诱导细胞外信号调节激酶(ERK)/p38/小眼畸形相关转录因子(MITF)激活,但不影响皮肤光型III的人表皮黑素细胞的黑素生成。UVB照射(20 mJ/cm²,持续5天)诱导皮肤光型III的黑素细胞发生黑素生成以及c-jun氨基末端激酶(JNK)/p38/MITF/酪氨酸酶激活。与单独的UVB相比,UVB与热联合处理导致皮肤光型III的黑素细胞中酪氨酸酶激活和黑素生成更为显著。此外,热处理和UVB照射诱导皮肤光型I的黑素细胞发生JNK、ERK和p38激活,但未引起黑素生成和形态学变化。这些发现提示,热可能通过热诱导的ERK/p38/MITF激活促进黑素细胞分化。此外,热对UVB诱导的酪氨酸酶激活和黑素生成具有叠加效应。这些结果为皮肤科医生利用热联合UVB照射治疗色素减退性皮肤病提供了新线索。