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Melanocytes do not migrate directionally in physiological DC electric fields
Author(s) -
Grahn Jennifer C.,
Reilly Debra A.,
Nuccitelli Richard L.,
Isseroff R. Rivkah
Publication year - 2003
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1046/j.1524-475x.2003.11110.x
Subject(s) - electric field , motility , wound healing , cell migration , melanocyte , biophysics , biology , chemistry , anatomy , microbiology and biotechnology , cell , immunology , physics , biochemistry , cancer research , melanoma , quantum mechanics
Wounding skin generates an endogenous electric field of 100–200 mV/mm in the immediate vicinity of the wound. When keratinocytes are exposed to direct current electric fields of this magnitude, they exhibit galvanotaxis, or directional migration toward the cathode, suggesting that wound‐generated electric fields provide migrational cues that contribute to wound healing. Because melanocytes must also migrate into the healing wound to repigment it, their motility in response to electric fields of physiologic magnitude was examined. Human skin–derived melanocytes, either exposed to 100 mV/mm direct current electric fields or nonexposed controls, both exhibited motility rates of 9 µm/hour, significantly (three‐ to five‐fold) lower than the motility rates of keratinocytes under identical conditions. However, in sharp contrast to keratinocytes, melanocytes exhibited no directional migration in the electric field. Additionally, neither the number of primary dendrites per cell, nor the orientation of the dendrites with respect to the field vector, nor the average length of the dendrites was significantly different in melanocytes exposed to the electric field as compared to nonexposed controls. Thus, in marked contrast to keratinocytes, human skin–derived melanocytes do not respond to direct current electric fields of physiologic magnitude with either directional migration or reorientation of dendrites. This may account for the delay in repigmentation that often accompanies wound reepithelialization. (WOUND REP REG 2003;11:64–70)