Abstract
The Teslar is a facial massager that emits a weak electric current, where users have reported a beneficial effect on skin elasticity with continued use. Accordingly, we conducted a clinical utility study and a comprehensive gene analysis, with cultured human fibroblasts to investigate the utility and mechanism of this treatment. In this clinical utility study, we found significant improvement in skin elasticity in Teslar treatments, compared to controls after two weeks of treatment. In cell experiments, we found that adenosine triphosphate synthesis and collagen contraction were promoted in fibroblasts cultured in type I collagen gel, following Teslar treatment. We considered that Teslar treatment exerted a structurally regenerative effect on the dermal matrix, based on the results of GeneChip® Expression Analysis. In particular, we demonstrated that Teslar treatment promotes type I collagen mRNA expression and fibulin-5/DANCE (Developmental arteries and neural crest EGF (epidermal growth factor)-like) mRNA expression and protein levels, which are reduced with aging. We also found increases in LTBP-3 (Latent TGF-β binding protein-3) and CSPG4 (Chondroitin sulfate proteoglycan 4) mRNA expression levels. Based on these results, we considered that Teslar treatment promoted dermal regeneration and recovery of skin elasticity.
Highlights
Skin cells have poor tensile strength and are vulnerable to pressure, and the surrounding extracellular matrix provides a strong, elastic tissue for support
We considered that the Teslar-induced increases in monocyte chemoattractant protein 1 (MCP-1) led to increases in transforming growth factor-β (TGF-β), chondroitin sulfate followed by collagen and elastin
We considered that Teslar treatment increased MCP-1 mRNA, which was followed by an increase in TGF-β1 mRNA, latent-transforming growth factor beta-binding protein (LTBP)-3-driven mobilization of TGF-β, and regulation of TGF-β activity through increased matrix metalloproteinase-14 (MMP-14) expression, increased chondroitin 6-sulfate and fibulin-5/DANCE, and activation of type I, IV, and XV collagen and insulin-like growth factor (IGF)
Summary
Skin cells have poor tensile strength and are vulnerable to pressure, and the surrounding extracellular matrix provides a strong, elastic tissue for support. Elastic fiber turnover is very slow, similar to that for collagen fibers [3,4]. They deteriorate with age, causing loss of dermal elasticity. This loss of dermal elasticity causes the skin to sag and lose its elasticity. Age-induced deterioration and elastic fiber breakdown render the skin unable to expand and contract, which is considered the direct cause of sagging and loss of elasticity. The fundamental solution for these issues involves reconstruction of elastic fibers
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