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Linking αMSH with PPARγ in B16‐F10 melanoma
Author(s) -
Maresca Vittoria,
Flori Enrica,
Camera Emanuela,
Bellei Barbara,
Aspite Nicaela,
Ludovici Matteo,
Catricalà Caterina,
Cardinali Giorgia,
Picardo Mauro
Publication year - 2013
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/j.1755-148x.2012.01042.x
Subject(s) - peroxisome proliferator activated receptor , receptor , signal transduction , endocrinology , nuclear receptor , medicine , transcription factor , melanocyte stimulating hormone , chemistry , microbiology and biotechnology , forskolin , biology , cancer research , biochemistry , gene
Summary We have discovered a new α‐melanocyte stimulating hormone (α‐MSH)/peroxisome proliferator activated receptor‐γ (PPAR‐γ) connection in B16‐F10 cells. Both PPAR‐γ up‐regulation and its induction as an active transcription factor were observed in response to α‐MSH. The α‐MSH/PPAR‐γ connection influenced both pigmentation and proliferation. The forskolin‐stimulated cAMP/PKA pathway was not able to induce either PPAR‐γ translocation into the nucleus or PPAR‐γ transcriptional activity. As the melanocortin‐1 receptor, the specific receptor for the α‐MSH, is a G‐protein coupled receptor, we wondered whether the phosphatidylinositol [PI(4,5)P 2 /PLC β ] signal pathway was involved in mediating the α‐MSH‐dependent PPAR‐γ activation. Employing inhibitors of PI(4,5)P 2 /PLC β pathway, the results of our experiments suggested that this pathway was promoted by α‐MSH and that α‐MSH played a role in mediating PPAR‐γ activation. We have demonstrated, for the first time, that α‐MSH induces the PI(4,5)P 2 /PLC β pathway, through analysis of the basic steps of the pathway. The α‐MSH effect on PPAR‐γ was independent of animal species and was not correlated with the physio‐pathological status.