Electric currents of 448 kHz upregulate anti‐senescence pathways in human dermal fibroblasts

Author:

Toledano‐Macías Elena1,Martínez‐Pascual María Antonia1,Hernández‐Bule María Luisa1ORCID

Affiliation:

1. Bioelectromagnetic Laboratory Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS) Madrid Spain

Abstract

AbstractBackgroundCurrently, finding new therapeutic strategies that reduce skin aging is a challenge for dermatologists and aesthetic doctors. In recent years, physical therapies have been included in the options for antiaging treatments; however, the biological bases of such treatments have scarcely been studied. One of these physical therapies is capacitive–resistive electric transfer (CRET) therapy. Previous studies have shown that subthermal treatment with CRET promotes the proliferation and migration of various cell types involved in skin regeneration, such as human ADSC (stem cells), fibroblasts, or keratinocytes.ObjectiveThis study investigates the effects of in vitro treatment with CRET‐Std (standard, non‐modulated signal) or CRET‐Mod (modulated signal) on cell proliferation and migration, markers of aging, and extracellular matrix production.MethodsThree types of human dermal fibroblasts were used: neonatal fibroblasts (HFn), replicative senescent fibroblasts (HFs), and adult fibroblasts (HFa). The effects of electric stimulation on cell proliferation and migration were studied through XTT and wound closure assays, respectively. The expression of the aging marker β‐galactosidase was assessed using a colorimetric assay, whereas immunoblot, immunofluorescence, and ELISAs were carried out to analyze the expression levels of migration, aging, and extracellular matrix proteins.ResultsThe treatment with CRET‐Std increased HFn and HFa proliferation, as well as migration in the three types of fibroblasts studied compared to those of the controls. Conversely, CRET‐Mod did not modify either of these two processes with respect to the controls. Additionally, CRET‐Std also reduced the cellular senescence markers β‐gal, vimentin, p53, and p21 in all three types of human skin fibroblasts. In addition, the application of CRET‐Std also induced fibronectin production in HFn and was able to stimulate ECM neocollagenesis.ConclusionCRET treatment improves a number of functions related to migration and proliferation, and it reduces age‐related cellular changes in human dermal fibroblasts. Therefore, the use of this CRET therapy to reduce the signs of dermal aging and to promote tissue regeneration could be of interest.

Publisher

Wiley

Subject

Dermatology

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