LPS induces melanogenesis through p38 MAPK activation in human melanocytes
LPS induces melanogenesis through p38 MAPK activation in human melanocytes
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DOI：
10.1007/s00403-008-0863-0
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发表时间：
2008-07-01
影响因子：
3
通讯作者：
Kang, Hee Young
中科院分区：
文献类型：
--
作者：
Ahn, Joo Hee;Jin, Sun Hee;Kang, Hee Young
我们已经观察到，脂多糖（LPS）诱导色素沉着的黑素细胞，并在这项研究中已经研究了这些反应是否介导的p38丝裂原活化蛋白激酶（MAPK）信号通路。LPS似乎刺激黑素细胞和培养皮肤的色素沉着。LPS可诱导小眼症相关转录因子（MITF）和酪氨酸酶蛋白的表达。用LPS刺激黑素细胞导致p38 MAPK的时间依赖性磷酸化。此外，p38 MAPK功能调节LPS诱导的黑色素形成的黑色素细胞; p38 MAPK抑制剂，SB 203580，几乎完全衰减LPS介导的上调黑色素合成和诱导MITF和酪氨酸酶的表达。这些结果表明，p38 MAPK的激活起着重要的作用，通过上调MITF和酪氨酸酶的表达在LPS诱导的黑素生成。
We have observed that lipopolysaccharide (LPS) induces pigmentation in melanocytes and in this study have examined whether these responses are mediated by the p38 mitogen-activated protein kinase (MAPK) signaling pathway. LPS appears to stimulate the pigmentation of melanocytes and cultured skin. LPS was found to induce the expression of microphthalmia-associated transcription factor (MITF) and tyrosinase protein in cells. Stimulation of melanocytes with LPS led to time dependent phosphorylation of p38 MAPK. Furthermore, p38 MAPK functionally regulated the LPS-induced melanin formation in melanocytes; a p38 MAPK inhibitor, SB203580, almost completely attenuated the LPS-mediated up-regulation of melanin synthesis and induction of MITF and tyrosinase expression. These findings indicate that activation of p38 MAPK plays an important role in LPS-induced melanogenesis by up-regulating MITF and tyrosinase expression.