Electrical stimulation promotes the proliferation of human keratinocytes, increases the production of keratin 5 and 14, and increases the phosphorylation of ERK1/2 and p38 MAP kinases

J Tissue Eng Regen Med. 2020 Jul;14(7):909-919. doi: 10.1002/term.3040. Epub 2020 May 27.

Abstract

Effective wound healing remains a significant clinical challenge in reducing patient morbidity and improving quality of life. Wound healing is a complex process involving the endogenous electrical field. The electrical field can contribute to wound healing by activating keratinocytes to promote reepithelialization. The objective of this study was to determine the effects of exogenous electrical stimulation (ES) on human keratinocyte viability and proliferation and on production of IL-6, IL-8, and keratins (K5 and K14) and to investigate the activated signalling pathways in keratinocytes exposed to ES. Keratinocytes were cultured under ES at different intensities for 6 or 24 hr. Cell proliferation, cytokines and growth factors, K5 and K14, as well as phosphorylated ERK1/2 and p38 MAP kinases, were evaluated. The results showed that the keratinocytes exposed to ES between 100 and 150 mV/mm for 6 or 24 hr showed a significantly increased proliferation rate. However, a 24 hr exposure to 200 mV/mm revealed no significant effect in cell growth. ES at 100 and 200 mV/mm for 6 hr increased the secretion of epidermal growth factor and vascular endothelial growth factor, and the production of K5 and K14. K14 was more sensitive than K5 to ES. However, ES down-regulated the secretions of IL-6 and IL-8. Finally, ES increased the phosphorylation of ERK1/2 and p38 MAP kinases. Overall results suggested that ES can be useful in supporting skin wound healing by activating keratinocytes.

Keywords: ERK1/2; conductive polymer; electrical stimulation; keratinocytes; keratins; p38; signalling; wound healing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Electric Stimulation
  • Female
  • Gene Expression Regulation*
  • Humans
  • Keratin-14 / biosynthesis*
  • Keratin-5 / biosynthesis*
  • Keratinocytes / metabolism*
  • MAP Kinase Signaling System*
  • Male
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Phosphorylation
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • KRT14 protein, human
  • KRT5 protein, human
  • Keratin-14
  • Keratin-5
  • MAPK1 protein, human
  • MAPK3 protein, human
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • p38 Mitogen-Activated Protein Kinases

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