Abstract
Pigmentation may result from melanocyte proliferation, melanogenesis, migration or increases in dendricity. Recently, it has been reported that secreted phospholipase A(2)(sPLA(2)) 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 PLA(2) activation. 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.
Highlights
Normal human melanocytes are located in the basal layer of the epidermis and rarely undergo mitosis (Jimbow et al, 1975; Pawelek, 1979)
We demonstrated that bee venom (BV) induces human melanocyte proliferation, melanogenesis, dendricity and migration
We demonstrated that treatment with BV causes a dose-dependent increase in melanocyte cell number as much as forskolin did and this proliferation lasted for 7 days (Figure 1B)
Summary
Normal human melanocytes are located in the basal layer of the epidermis and rarely undergo mitosis (Jimbow et al, 1975; Pawelek, 1979). TPA acts on melanocyte growth through activation of PKC (Arita et al, 1992), whereas ET-1 and bFGF may affect melanocyte growth through phosphorylation of ERK 1/2 (Swope et al, 1995; Tada et al, 2002). Activation of ERK1/2 is critical for the mitogenic response of melanocytes. Failure to activate this kinase is evident in terminally differentiated melanocytes (Medrano et al, 1994). Activation of ERK1/2 is sequentially connected to cAMP response element binding protein (CREB) activation (Tada et al, 2002). CREB could be a common downstream target for melanocyte differentiation and proliferation
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