ABSTRACT
Directional cellular locomotion is thought to involve localized intracellular calcium changes and the lateral transport of cell surface molecules. Brown et al. (26) examined the roles of both calcium and cell surface glycoprotein redistribution in the directional migration of two murine fibroblastic cell lines, in contrast to human dermal fibroblast result reported by Sillman et al. (25) and directional migration of NIH 3T3 and SV101. These cell types exhibit persistent, cathode-directed motility when exposed to direct current electric fields. Using time lapse phase contrast microscopy and image analysis, we have determined that electric field-directed locomotion in each cell type is a calcium-independent process. Both exhibit cathode-directed motility in the absence of extracellular calcium, and electric fields cause no detectable elevations or gradients of cytosolic free calcium. On the basis of the evidence, the authors suggested that galvanotaxis in these cells involves the lateral redistribution of plasma membrane glycol proteins. Electric fields cause the lateral migration of plasma membrane concanavalin A (Con A) receptors toward the cathode in both NIH 3T3 and SV101 fibroblasts. Exposure of directionally migrating cells to Con A inhibits the normal change of cell direction following a reversal of electric field polarity. Additionally, when cells are plated on Con A-coated substrata so that Con A receptors mediate cell-substratum adhesion, cathodedirected locomotion, and a cathodal accumulation of Con A receptors are observed. Immunofluorescent labeling of the fibronectin receptor in NIH 3T3 fibroblasts suggests the recruitment of integrins from large clusters to form a more diffuse distribution toward the cathode in field-treated cells. It was concluded that the mechanism of electric field-directed locomotion in NIH 3T3 and SV101 fibroblasts involves the lateral redistribution of plasma membrane glycol proteins involved in cell substratum adhesion.
