Radiofrequency Currents Modulate Inflammatory Processes in Keratinocytes.
Humans
Keratinocytes
/ metabolism
NF-kappa B
/ metabolism
Cell Proliferation
Cytokines
/ metabolism
Matrix Metalloproteinase 9
/ metabolism
Inflammation
/ metabolism
Radio Waves
ErbB Receptors
/ metabolism
HaCaT Cells
Matrix Metalloproteinase 1
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
MAP Kinase Signaling System
Cell Line
EGFR
ERK1/2
MMPs
NF-κB
cytokine
inflammation
keratinocyte
physical therapies
radiofrequency
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
03 Oct 2024
03 Oct 2024
Historique:
received:
02
08
2024
revised:
30
09
2024
accepted:
01
10
2024
medline:
16
10
2024
pubmed:
16
10
2024
entrez:
16
10
2024
Statut:
epublish
Résumé
Keratinocytes play an essential role in the inflammatory phase of wound regeneration. In addition to migrating and proliferating for tissue regeneration, they produce a large amount of cytokines that modulate the inflammatory process. Previous studies have shown that subthermal treatment with radiofrequency (RF) currents used in capacitive resistive electric transfer (CRET) therapy promotes the proliferation of HaCat keratinocytes and modulates their cytokine production. Although physical therapies have been shown to have anti-inflammatory effects in a variety of experimental models and in patients, knowledge of the biological basis of these effects is still limited. The aim of this study was to investigate the effect of CRET on keratinocyte proliferation, cytokine production (IL-8, MCP-1, RANTES, IL-6, IL-11), TNF-α secretion, and the expression of MMP9, MMP1, NF-κB, ERK1/2, and EGFR. Human keratinocytes (HaCat) were treated with an intermittent 448 kHz electric current (CRET signal) in subthermal conditions and for different periods of time. Cell proliferation was analyzed by XTT assay, cytokine and TNF-α production by ELISA, NF-κB expression and activation by immunofluorescence, and MMP9, MMP1, ERK1/2, and EGF receptor expression and activation by immunoblot. Compared to a control, CRET increases keratinocyte proliferation, increases the transient release of MCP-1, TNF-α, and IL-6 while decreasing IL-8. In addition, it modifies the expression of MMPs and activates EGFR, NF-κB, and ERK1/2 proteins. Our results indicate that CRET reasonably modifies cytokine production through the EGF receptor and the ERK1/2/NF-κB pathway, ultimately modulating the inflammatory response of human keratinocytes.
Identifiants
pubmed: 39408993
pii: ijms251910663
doi: 10.3390/ijms251910663
pii:
doi:
Substances chimiques
NF-kappa B
0
Cytokines
0
Matrix Metalloproteinase 9
EC 3.4.24.35
ErbB Receptors
EC 2.7.10.1
Matrix Metalloproteinase 1
EC 3.4.24.7
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : This research was funded by INDIBA S.A. and by the Fundación para la Investigación Biomédica del Hospital Universitario Ramón y Cajal
ID : Project FiBio-HRC No. 2015/0050