Ota A, Park J S, Jimbow K
Dermatology and Cutaneous Sciences, Faculty of Medicine, University of Alberta, Edmonton, Canada.
Br J Dermatol. 1998 Aug;139(2):207-15. doi: 10.1046/j.1365-2133.1998.02356.x.
This study characterizes the induction of melanogenesis and the expression of tyrosinase, tyrosinase-related protein (TRP) and lysosome-associated membrane protein (LAMP) gene families in the cultured melanocyte lines of non-agouti mice with four major genetic loci, i.e. melan-a2 (black, wild type), melan-b (brown, TRP-1 mutation), melan-s (black, piebaldism mutation) and melan-c (white, tyrosinase mutation) in response to repeated exposure to ultraviolet (UV) B (5 mJ/cm2, 7 consecutive days). Electron microscopy showed that new melanogenesis was induced in melan-a2, melan-s and melan-b melanocytes. Melan-a2, melan-s and melan-b showed an almost twofold increase in tyrosinase activity and gene expression with increased synthesis of melanosomes, although melan-b showed a minimum increase in tyrosinase activity. There was a twofold upregulation of LAMP-1 mRNA but no alteration in LAMP-2 and LAMP-3 mRNA expression in melan-a2, while there was no alteration in LAMP-1 mRNA expression but increased expression of LAMP-2 and LAMP-3 mRNA in melan-s, LAMP-3 showing a higher increase. Melan-b cells showed the same gene expression of LAMP-1, LAMP-2 and LAMP-3 as that of non-UV exposed cells. All three lines, however, exhibited simultaneously cell death, melan-b reaching the highest rate of cell death (96.5%). In contrast, melan-c, which did not have any tyrosinase activity with failure of melanogenesis induction, expressed all the mRNAs of the tyrosinase and LAMP gene families, but was not associated with any significant melanocyte death. Our study indicated: (i) that melanogenesis induction and melanocyte death are two photobiological processes occurring simultaneously after repeated UVB exposure, (ii) that in response to an upregulation of tyrosinase mRNA and enzymic activity, there was a co-ordinated upregulation of the LAMP-1 gene in wild type melan-a2, while no upregulation was found in melan-s and melan-b mutants, and (iii) that UV-induced melanocyte death is related to the upregulation of the tyrosinase gene, induction of new melanogenesis and mutation of the TRP-1 gene in immortal murine melanocytes.
本研究对具有四个主要基因位点的非刺豚鼠小鼠培养黑素细胞系中黑色素生成的诱导以及酪氨酸酶、酪氨酸酶相关蛋白(TRP)和溶酶体相关膜蛋白(LAMP)基因家族的表达进行了表征,这四个基因位点分别为黑素-a2(黑色,野生型)、黑素-b(棕色,TRP-1突变)、黑素-s(黑色,花斑突变)和黑素-c(白色,酪氨酸酶突变),研究其对重复暴露于紫外线(UV)B(5 mJ/cm2,连续7天)的反应。电子显微镜显示,黑素-a2、黑素-s和黑素-b黑素细胞中诱导了新的黑色素生成。黑素-a2、黑素-s和黑素-b的酪氨酸酶活性和基因表达几乎增加了两倍,同时黑素小体合成增加,尽管黑素-b的酪氨酸酶活性增加最少。黑素-a2中LAMP-1 mRNA上调了两倍,但LAMP-2和LAMP-3 mRNA表达没有改变,而黑素-s中LAMP-1 mRNA表达没有改变,但LAMP-2和LAMP-3 mRNA表达增加,LAMP-3增加幅度更高。黑素-b细胞中LAMP-1、LAMP-2和LAMP-3的基因表达与未暴露于紫外线的细胞相同。然而,所有三个细胞系都同时出现细胞死亡,黑素-b的细胞死亡率最高(96.5%)。相比之下,黑素-c没有任何酪氨酸酶活性,无法诱导黑色素生成,它表达了酪氨酸酶和LAMP基因家族的所有mRNA,但与任何显著的黑素细胞死亡无关。我们的研究表明:(i)重复暴露于UVB后,黑色素生成诱导和黑素细胞死亡是两个同时发生的光生物学过程;(ii)响应酪氨酸酶mRNA和酶活性的上调,野生型黑素-a2中LAMP-1基因协同上调,而黑素-s和黑素-b突变体中未发现上调;(iii)紫外线诱导的黑素细胞死亡与酪氨酸酶基因的上调、新黑色素生成的诱导以及永生小鼠黑素细胞中TRP-1基因的突变有关。