Melanocyte distribution and function in human skin -: Effects of ultraviolet radiation
Melanocyte distribution and function in human skin -: Effects of ultraviolet radiation
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DOI：
10.1007/978-1-59259-994-3_6
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发表时间：
2006-01-01
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影响因子：
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通讯作者：
Hearing, Vincent J.
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文献类型：
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作者：
Yamaguchi, Yuji;Hearing, Vincent J.
参与黑色素合成的催化实体(包括酪氨酸酶[TYR]、酪氨酸酶相关蛋白1[TYRP1]和多巴色素互变异构酶[DCT])和对黑素小体完整性至关重要的结构蛋白(包括GP100/PMel17)在维持黑素细胞产生的细胞器的功能和结构方面发挥着积极的作用。结构性皮肤色素沉着受多种不同因素的调节(包括黑素细胞的树突、黑素小体向树突的运输、黑素小体向角质形成细胞的转移及其随后的分布)，并可受旁分泌因子(来自邻近的角质形成细胞和成纤维细胞)和环境(包括紫外线(UV)辐射)的影响，这些因素调节黑素细胞的增殖和功能。由于紫外线本身与皮肤光癌(包括黑色素瘤)有关，我们讨论了三种不同类型的皮肤对紫外线的反应，包括黑素细胞密度和功能、黑色素含量和分布、DNA损伤(通过6，4-植物产物[64pp]和环丁烷嘧啶二聚体[CPD]测量)和细胞凋亡(通过末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记[TUNEL]染色测量)。综上所述，在浅色/白皙皮肤中，紫外线诱导的下表皮DNA损伤不能被有效地防止，在低剂量紫外线照射后，紫外线诱导的细胞凋亡在浅色皮肤中看不到。这些观察表明，DNA损伤的减少和紫外线损伤细胞的更有效去除相结合，在深色皮肤中减少光癌起到了重要作用。
Catalytic entities involved in melanin synthesis (including tyrosinase [TYR], tyrosinase-related protein 1 [TYRP1], and dopachrome tautomerase [DCT]) and structural proteins important to the integrity of melanosomes (including GP100/Pmel17) play active roles in the maintenance of the function and structure of those organelles produced by melanocytes. Constitutive skin pigmentation is regulated by a number of distinct factors (including melanocyte dendricity, transport of melanosomes to dendrites, and transfer of melanosomes to keratinocytes and their subsequent distribution) and can be affected by paracrine factors (from neighboring keratinocytes and fibroblasts) and the environment, including ultraviolet (UV) radiation, that regulate melanocyte proliferation and function. Because UV is inherently associated with photocarcinogenesis in the skin, including melanoma, we discuss melanocyte density and function, melanin content and distribution, DNA damage (measured by 6,4-phytoproducts [64PP] and cyclobutane pyrimidine dimers [CPD]) and apoptosis (measured by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling [TUNEL] staining) in response to UV in three different types of skin. In sum, UV-induced DNA damage in the lower epidermis is not effectively prevented in light/fair skin and UV-induced apoptosis is not seen in light skin after low doses of UV. These observations suggest that the combination of decreased DNA damage and more efficient removal of UV-damaged cells plays an important role in the decreased photocarcinogenesis seen in darker skin.