Activation of p38 or p44/42 mitogen-activated protein (MAP) kinases has been shown to trigger differentiation in a number of cell types. The present study has investigated the roles of these kinases in the alpha-melanocyte stimulating hormone (alpha-MSH)-induced melanogenic and proliferative responses in B16 melanoma cells. Treatment of cells with alpha-MSH led to the time-dependent phosphorylation of both p38 and p44/42 MAP kinases. However, only inhibition of p38 MAP kinase activity with SB 203580 blocked both the alpha-MSH-induced melanogenic and anti-proliferative effects. It therefore appears that activation of the p38 pathway can promote melanogenesis and inhibit growth of B16 melanoma cells.
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Article Synopsis
- MC1R is a receptor in melanocytes that regulates melanin production via α-MSH, while TLR4, found in various cell types, activates immune responses and also enhances melanin production through the NF-κB pathway.
- Benzimidazole-2-butanol (BI2B) has been identified as an inhibitor of the LPS/TLR4 pathway and shows potential in reducing excess pigmentation by targeting the α-MSH-induced melanogenic process.
- In tests involving UV-B-irradiated mouse skin and activated melanocyte cultures, BI2B effectively decreased levels of melanogenic markers and disrupted key signaling pathways linked to pigmentation, highlighting its role in managing hyperpigmentation.
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