Electrical stimulation (ES) is known to promote cutaneous healing, however its ability to regulate reinnervation remains unclear. Firstly, we show that ES treatment of human acute cutaneous wounds (n=40) increased reinnervation. Next, to define neurophysiological mechanisms through which ES impacts repair, microarray of wound biopsies was performed on days 3, 7, 10 and 14 post-wounding. This identified neural differentiation biomarkers Class III β-tubulin (TUBB3; melanocyte development and neuronal marker) and its upstream molecule Factor Induced Gene 4 (FIG4; phosphatidylinositol (3,5)-bisphosphate 5-phosphatase) as significantly up-regulated post-ES treatment. To demonstrate a functional ES-TUBB3 axis in cutaneous healing, we showed increased TUBB3(+) melanocytes and melanogenesis plus FIG4 and nerve growth factor expression, suggesting higher cellular differentiation. In supporting this role of ES to regulate neural-crest derived cell fate and differentiation in vivo, knock down of FIG4 in neuroblastoma cells resulted in vaculogenesis and cell degeneration, while ES treatment post FIG4-siRNA transfection enhanced neural differentiation, survival and integrity. Further characterisation showed increased TUBB3(+) and PGP9.5(+) Merkel cells during in vivo repair, post-ES. We demonstrate that ES contributes to increased expression of neural differentiation biomarkers, reinnervation and expansion of melanocyte and Merkel cell pool during repair. Targeted ES-assisted acceleration of healing has significant clinical implications.
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 07 April 2018.
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