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β‐Catenin regulates melanocyte dendricity through the modulation of PKCζ and PKCδ
Author(s) -
Kim JinHwa,
Sohn KyungCheol,
Choi TaeYoung,
Kim Mi Yoon,
Ando Hideya,
Choi Sun Ja,
Kim Sooil,
Lee Young Ho,
Lee JeungHoon,
Kim Chang Deok,
Yoon TaeJin
Publication year - 2010
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.2010.00695.x
Subject(s) - microbiology and biotechnology , wnt signaling pathway , protein kinase c , catenin , rac1 , cdc42 , chemistry , signal transduction , melanocyte , biology , cancer research , melanoma
Summary The Wnt/β‐catenin signaling pathway is involved in the melanocyte differentiation and melanoma development. However, the effect of β‐catenin for dendrite formation has not been clearly elucidated yet in normal human epidermal melanocytes (NHEM). To investigate the effect of β‐catenin, we transduced NHEM with recombinant adenovirus expressing β‐catenin. Forced expression of β‐catenin led to the dramatic morphological changes of NHEM, including the reduction of dendrite length and enlargement of cell body. Concomitantly with, the protein levels for dendrite formation‐related molecules, such as Rac1 and Cdc42, were markedly decreased. In addition, phosphorylation of p38 MAPK was significantly reduced by β‐catenin, potentiating its inhibitory role for dendrite formation. Interestingly, overexpression of β‐catenin led to the increase of protein kinase C ζ (PKCζ) level, while protein kinase C δ (PKCδ) was decreased by β‐catenin, suggesting that those PKCs were β‐catenin‐downstream modulators in NHMC. When PKCζ was overexpressed, dendrites were shortened, with the reduced protein levels for Rac1 and Cdc42. In contrast, PKCδ overexpression led to the elongation of dendrites, with the increased levels for Rac1 and Cdc42. These results suggest that β‐catenin play an inhibitory role for dendrite formation through the modulation of PKCζ and PKCδ.