Bee venom stimulates human melanocyte proliferation, melanogenesis, dendricity and migration.
- Author:
Songhee JEON
1
;
Nan Hyung KIM
;
Byung Soo KOO
;
Hyun Joo LEE
;
Ai Young LEE
Author Information
1. Dongguk University Research Institute of Biotechnology, Medical Science Research Center, Goyang 410-773, Korea. leeay@duih.org
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
bee venoms;
cell movement;
cell proliferation;
melanocytes;
melanins;
skin pigmentation;
vitiligo
- MeSH:
Animals;
Base Sequence;
Bee Venoms/*pharmacology;
Cell Movement/drug effects;
Cell Proliferation/drug effects;
Cells, Cultured;
Cyclic AMP/metabolism;
DNA Primers/genetics;
Forskolin/pharmacology;
Gene Expression/drug effects;
Humans;
Melanins/biosynthesis;
Melanocytes/cytology/*drug effects/physiology;
Microphthalmia-Associated Transcription Factor/biosynthesis/genetics;
Monophenol Monooxygenase/biosynthesis/genetics;
Signal Transduction/drug effects
- From:Experimental & Molecular Medicine
2007;39(5):603-613
- CountryRepublic of Korea
- Language:English
-
Abstract:
Pigmentation may result from melanocyte proliferation, melanogenesis, migration or increases in dendricity. Recently, it has been reported that secreted phospholipase A2(sPLA2) known as a component of bee venom (BV), stimulates melanocyte dendricity and pigmentation. BV has been used clinically to control rheumatoid arthritis and to ameliorate pain via its anti-inflammatory and antinociceptive properties. Moreover, after treatment with BV, pigmentation around the injection sites was occasionally observed and the pigmentation lasted a few months. However, no study has been done about the effect of BV on melanocytes. Thus, in the present study, we examined the effect of BV on the proliferation, melanogenesis, dendricity and migration in normal human melanocytes and its signal transduction. BV increased the number of melanocytes dose and time dependently through PKA, ERK, and PI3K/Akt activation. The level of cAMP was also increased by BV treatment. Moreover, BV induced melanogenesis through increased tyrosinase expression. Furthermore, BV induced melanocyte dendricity and migration through PLA2activation. Overall, in this study, we demonstrated that BV may have an effect on the melanocyte proliferation, melanogenesis, dendricity and migration through complex signaling pathways in vitro, responsible for the pigmentation. Thus, our study suggests a possibility that BV may be developed as a therapeutic drug for inducing repigmentation in vitiligo skin.
