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Published on: June 7, 2019
Human placental lipid induces melanogenesis through p38 MAPK in B16F10 mouse melanoma
Suman Kumar Singh1, Chinmoy Sarkar, Shampa Mallick
1Department of Cellular Biochemistry, Indian Institute of Chemical Biology, 4, Raja S.C. Mullick Road, Jadavpur, Kolkata-700 032, India.
Abstract:
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.
Insights
Placental total lipid fraction stimulates melanogenesis by activating p38 mitogen-activated protein kinase (MAPK) signaling, which upregulates tyrosinase expression in melanoma cells. Inhibiting p38 MAPK blocks this effect, highlighting its crucial role.
Area of Science:
- Biochemistry
- Cell Biology
- Dermatology
Background:
- Melanogenesis, crucial for melanocyte/melanoma function, is regulated by MAPK and Akt/PKB pathways.
- Placental total lipid fraction (PTLF), rich in sphingolipids, stimulates melanogenesis by upregulating tyrosinase in B16F10 melanoma cells.
Purpose of the Study:
- To investigate the roles of MAPK and Akt/PKB pathways in PTLF-induced melanogenesis and tyrosinase expression in B16F10 melanoma cells.
Main Methods:
- Cells were treated with PTLF, and phosphorylation of p38 MAPK was assessed.
- Inhibitors of p38 MAPK (SB203580), PI3K (LY294002), and MEK (PD98059) were used to study pathway involvement.
- Tyrosinase promoter activity and expression were measured.
Main Results:
- PTLF induced time-dependent phosphorylation of p38 MAPK.
- Inhibition of p38 MAPK completely blocked PTLF-induced melanogenesis and tyrosinase expression.
- Inhibitors of Akt/PKB and MEK pathways potentiated PTLF-induced p38 MAPK phosphorylation, tyrosinase expression, and melanogenesis.
Conclusions:
- Activation of the p38 MAPK pathway is critical for PTLF-induced melanogenesis in B16F10 melanoma cells.
- p38 MAPK activation upregulates tyrosinase expression, mediating the pigmentation effects of PTLF.
