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Abstract
Wound healing constitutes an essential process for all organisms and involves a sequence of three phases. The disruption or elongation of any of these phases can lead to a chronic or non-healing wound. Electrical stimulation accelerates wound healing by mimicking the current that is generated in the skin after any injury. Here, we sought to identify the molecular mechanisms involved in the healing process following in vitro microcurrent stimulation—a type of electrotherapy. Our results concluded that microcurrents promote cell proliferation and migration in an ERK 1/2- or p38-dependent way. Furthermore, microcurrents induce the secretion of transforming growth factor-beta-1 (TGF-β1) in fibroblasts and osteoblast-like cells. Interestingly, transcriptomic analysis uncovered that microcurrents enhance the transcriptional activation of genes implicated in Hedgehog, TGF-β1 and MAPK signaling pathways. Overall, our results demonstrate that microcurrents may enhance wound closure through a combination of signal transductions, via MAPK’s phosphorylation, and the transcriptional activation of specific genes involved in the healing process. These mechanisms should be further examined in vivo, in order to verify the beneficial effects of microcurrents in wound or fracture healing.
Highlights
The ability of an organism to respond to injury, in order to achieve tissue repair and to maintain homeostasis, is of high significance [1,2]
To identify whether the microcurrents activate specific signaling pathways in mammalian cells, we examined the phosphorylation of ERK 1/2 and p38 kinases in two different cell lines: NIH3T3 and MG-63
NIH3T3 cells are mouse embryonic fibroblasts, which participate in all three phases of wound healing by mediating several important activities for wound closure [34,35]
Summary
The ability of an organism to respond to injury, in order to achieve tissue repair and to maintain homeostasis, is of high significance [1,2]. Acute wounds normally heal in a steady and efficient way, consisting of three distinct but overlapping phases: inflammation, tissue formation and remodeling [1,2,3,4,5]. Different cell types, such as macrophages, neutrophils, keratinocytes, fibroblasts, endothelial cells etc., are recruited and interact with each other to restore the damaged tissue area [1,3,6,7,8]. Impairment in one or more of these phases leads to delayed wound healing or to a chronic, non-healing wound [9,10]. Parts of the injured areas are found in different stages of healing or are “trapped” in a certain phase for a prolonged period [3,9]. The molecular mechanisms that lead to ineffective wound healing are not clearly elucidated
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