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首页> 外文期刊>Pigment cell research >Human placental lipid induces melanogenesis through p38 MAPK in B16F10 mouse melanoma
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Human placental lipid induces melanogenesis through p38 MAPK in B16F10 mouse melanoma

机译：人胎盘脂质通过B16F10小鼠黑色素瘤中的p38 MAPK诱导黑色素生成

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Melanogenesis is one of the characteristic functional activities of melanocyte/melanoma and is regulated via mitogen-activated protein kinase (MAPK) and Akt/protein kinase B (PKB) pathways. Placental total lipid fraction (PTLF), prepared from a hydroalcoholic extract of fresh term human placenta contains sphingolipids and was recently shown to stimulate melanogenesis via up-regulation of the key enzyme tyrosinase in B16F10 mouse melanoma cells. How such lipids mediate their effects on pigmentation and tyrosinase expression is a particularly important aspect of melanogenesis. To study the signaling that leads to tyrosinase expression, we have investigated the roles of the MAPK and Akt/PKB pathways in B16F10 melanoma cells in melanogenesis in response to PTLF. Treatment of cells with PTLF led to the time dependent phosphorylation of p38 MAPK. SB203580, a p38 MAPK inhibitor, completely blocked the PTLF-induced melanogenesis by inhibiting promoter activity and subsequent expression of tyrosinase. Phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002 a blocker of the Akt signaling pathway, or an inhibitor of MEK (MAPK/ERK Kinase), PD98059 when included along with PTLF was found to potentiate PTLF-induced phosphorylation of p38 MAPK together with tyrosinase expression and melanogenesis. The results suggest that the activation of p38 MAPK plays a crucial role in PTLF-induced B16F10 melanogenesis by up-regulating tyrosinase expression.
机译：黑色素生成是黑色素细胞/黑色素瘤的特征性功能活动之一，并通过有丝分裂原激活的蛋白激酶（MAPK）和Akt /蛋白激酶B（PKB）途径进行调控。由新鲜足月人胎盘的水醇提取物制备的胎盘总脂质级分（PTLF）包含鞘脂，最近被证明可通过上调B16F10小鼠黑素瘤细胞中关键酶酪氨酸酶来刺激黑素生成。这种脂质如何介导其对色素沉着和酪氨酸酶表达的影响是黑色素生成的一个特别重要的方面。为了研究导致酪氨酸酶表达的信号传导，我们研究了B16F10黑色素瘤细胞中MAPK和Akt / PKB通路在响应PTLF的黑色素生成中的作用。用PTLF处理细胞导致时间依赖性磷酸化p38 MAPK。 p38 MAPK抑制剂SB203580通过抑制启动子活性和酪氨酸酶的后续表达，完全阻断了PTLF诱导的黑色素生成。发现磷脂酰肌醇3激酶（PI3K）抑制剂，Akt信号通路的阻断剂LY294002或MEK（MAPK / ERK激酶）抑制剂PD98059当与PTLF一起使用时，可增强PTLF诱导的p38 MAPK与酪氨酸酶的磷酸化表达和黑色素生成。结果表明，通过上调酪氨酸酶表达，p38 MAPK的激活在PTLF诱导的B16F10黑色素生成中起关键作用。

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