未经证实:已经证明一氧化氮(NO)可以调节表皮黑素细胞的免疫特性,皮肤中NO的过度表达可能导致炎症相关的色素性疾病。关于组成型细胞色素沉着是否影响黑素细胞对NO的敏感性知之甚少。
UNASSIGNED:比较NO对不同程度组成型色素沉着的正常人黑素细胞中黑色素合成和关键黑色素生成相关基因表达的影响。
未经授权:人类表皮黑素细胞来自轻度和深色皮肤(HEMn-LP和HEMn-DP,分别)在有或没有NO供体(SPER/NO)的情况下培养。然后是黑色素的总含量,pheomelanin含量,酪氨酸酶的活性和浓度,并评估了TYR和DCT的表达。
未经证实:从SPER/NO释放的NO并没有改变培养细胞产生的黑色素的总量,但增加了苯黑素的比例,尤其是在HEMn-DP中。黑素生成相关基因的转录活性,特别是DCT,在用SPER/NO培养的HEMn-DP中下调,在HEMn-LP中上调。
未经证实:NO可以促进人表皮黑素细胞的黑色素生成,在这方面,细胞反应与色素沉着表型有关。在接触NO期间,来自深色皮肤的黑素细胞比浅色细胞产生更多的pheomelanin。NO诱导的皮肤中的pheomelanin的过量产生可能是导致深色皮肤个体发生严重炎症性皮肤病的更大倾向的因素之一。甚至基于局部慢性炎症的黑色素瘤从头形成。
UNASSIGNED: It has been shown that nitric oxide (NO) can modulate the immune properties of epidermal melanocytes, and that overexpression of NO in the skin may contribute to inflammation-related pigmentary disorders. Little is known about whether constitutive cell pigmentation affects the sensitivity of melanocytes to NO.
UNASSIGNED: To compare the effect of NO on melanin synthesis and the expression of key melanogenesis-related genes in normal human melanocytes of various degrees of constitutive pigmentation.
UNASSIGNED: Human epidermal melanocytes derived from lightly and darkly pigmented skin (HEMn-LP and HEMn-DP, respectively) were cultured with or without a NO donor (SPER/NO). Then the total melanin content, the
pheomelanin content, the activity and concentration of tyrosinase, and the expressions of TYR and DCT were assessed.
UNASSIGNED: NO released from SPER/NO did not alter the total amount of melanin produced by cultured cells but increased the proportion of
pheomelanin, especially in HEMn-DP. Transcriptional activity of the melanogenesis-related genes, in particular DCT, was downregulated in HEMn-DP and upregulated in HEMn-LP cultured with SPER/NO.
UNASSIGNED: NO can promote pheomelanogenesis in human epidermal melanocytes, and the cell response in this respect is associated with the pigmentation phenotype. During exposure to NO, melanocytes from dark skin produce much more
pheomelanin than lightly pigmented cells. NO-induced overproduction of
pheomelanin in the skin could be one of the factors responsible for the greater propensity to develop severe inflammatory dermatoses in dark-skinned individuals, or even melanoma de novo formation based on local chronic inflammation.