Abstract
This study evaluated frequency-dependent effects of extremely low frequency electromagnetic fields (ELF-EMFs) on melanogenesis by melanocytes in vitro. Melanocytes were exposed to 2 mT EMFs at 30–75 Hz for 3 days before melanogenesis was examined. Exposure to ELF-EMFs at 50 and 60 Hz induced melanogenic maturation without cell damage, without changing cell proliferation and mitochondrial activity. Melanin content and tyrosinase activity of cells exposed to 50 Hz were higher than in controls, and mRNA expression of tyrosinase-related protein-2 was elevated relative to controls at 50 Hz. Phosphorylated cyclic adenosine monophosphate response element-binding protein (p-CREB) levels were higher than controls in cells exposed to ELF-EMFs at 50–75 Hz. Immunohistochemical staining showed that melanocyte-specific markers (HMB45, Melan-A) were strongly expressed in cells exposed to EMFs at 50 and 60 Hz compared to controls. Thus, exposure to ELF-EMFs at 50 Hz could stimulate melanogenesis in melanocytes, through activation of p-CREB and p-p38 and inhibition of phosphorylated extracellular signal-regulated protein kinase and phosphorylated stress-activated protein kinase/c-Jun N-terminal kinase. The results may form the basis of an appropriate anti-gray hair treatment or be applied in a therapeutic device for inducing repigmentation in the skin of vitiligo patients.
Highlights
Melanocytes, which differentiate from melanoblasts, can produce the pigment melanin in a process called melanogenesis
Melanin is present in tissues, such as skin and hair, and in the eyes, and it is synthesized by the melanosome organelle within the melanocyte [1]
Melanin synthesis and pigment transfer to bulb keratinocytes are dependent on the availability of melanin precursors and regulation by signal transduction pathways intrinsic to skin and hair follicles, which are both receptor-dependent and -independent, act through auto, para- or intracrine mechanisms and can be modified by hormonal
Summary
Melanocytes, which differentiate from melanoblasts, can produce the pigment melanin in a process called melanogenesis. Melanin is present in tissues, such as skin and hair, and in the eyes, and it is synthesized by the melanosome organelle within the melanocyte [1]. The skin contains a local defensive melanocortin system to neutralize a wide range of external noxious stimuli (principally UVR) and consists of the pigment melanin and its associated cleaved proopiomelanocortin (POMC) peptides. UVR stimulates POMC formation, with resultant release of several POMC peptides via differential enzymatic cleavage of POMC by prohormone convertases. Corticotropin (ACTH), and α-, β-, and γ-melanocyte-stimulating hormones (MSHs) are produced that can influence melanogenesis. Melanin pigment synthesized in this way can act as a buffer molecule to antagonize the noxious effects of physical, biological, and chemical insults [3,4]
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