Soft tissue repair is a complex process that requires specific communication between multiple cell types to orchestrate effective restoration of physiological functions. Macrophages play a critical role in this wound healing process beginning at the onset of tissue injury. Understanding the signaling mechanisms involved in macrophage recruitment to the wound site is an essential step for developing more effective clinical therapies. Macrophages are known to respond to electrical fields, but the underlying cellular mechanisms mediating this response is unknown. This study demonstrated that low‐amplitude sine‐wave electrical stimulation (ES) initiates a soft tissue response in the absence of injury in Procambarus clarkii. This cellular response was characterized by recruitment of macrophage‐like hemocytes to the stimulation site indicated by increased hemocyte density at the site. ES also increased tissue collagen deposition compared to sham treatment (P < 0.05). Voltage‐gated potassium (KV) channel inhibition with either 4‐aminopyridine or astemizole decreased both hemocyte recruitment and collagen deposition compared to saline infusion (P < 0.05), whereas inhibition of calcium‐permeable channels with ruthenium red did not affect either response to ES. Thus, macrophage‐like hemocytes in P. clarkii elicit a wound‐like response to exogenous ES and this is accompanied by collagen deposition. This response is mediated by KV channels but independent of Ca2+ channels. We propose a significant role for KV channels that extends beyond facilitating Ca2+ transport via regulation of cellular membrane potentials during ES of soft tissue.

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Published in Physiological Reports, v. 4, issue 12, e12832, p. 1-10.

© 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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