Background Proliferation and differentiation of keratinocytes are central processes in tissue regeneration after injury. Chemokines, produced by a wide range of cell types including keratinocytes, play a regulatory role in inflammatory skin dis- eases. Several studies have shown that an electromagnetic field (EMF) can influ- ence both inflammatory processes and repair mechanisms including wound healing on different tissue models. Objectives To elucidate the effect of extremely low frequency EMF (ELF-EMF) on keratinocyte proliferation and production of chemokines [RANTES, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1a and interleukin (IL)-8] in order to evaluate a potential therapeutic use of mag- netic fields. Methods The human keratinocyte cell line HaCaT was exposed at 1 mT, 50 Hz for different lengths of time and compared with unexposed control cells. Cell growth and viability were evaluated at different exposure times by cell count and trypan blue exclusion. Chemokine production and expression were analysed by enzyme- linked immunosorbent assay (ELISA) and by real-time polymerase chain reaction. Total NF-jB p65 was quantified by ELISA. Results Significantly increased growth rates were observed after 48 h of EMF exposure as compared with control cells, while no difference in cell viabilities were detected. Gene expression and release of RANTES, MCP-1, MIP-1a and IL-8 were significantly reduced after 72 h of exposure. NF-jB levels became almost undetectable after only 1 h of EMF exposure, and were inversely correlated with cell density. Conclusions Our results show that ELF-EMF modulates chemokine production and keratinocyte growth through inhibition of the NF-jB signalling pathway and thus may inhibit inflammatory processes. ELF-EMF could represent an additional ther- apeutic approach in the treatment of skin injury.

Extremely low frequency electromagnetic field enhances human keratinocyte cell growth and decreases proinflammatory chemokine production

VIANALE, GIOVINA;REALE, Marcella;AMERIO, Paolo;MURARO, Raffaella
2008-01-01

Abstract

Background Proliferation and differentiation of keratinocytes are central processes in tissue regeneration after injury. Chemokines, produced by a wide range of cell types including keratinocytes, play a regulatory role in inflammatory skin dis- eases. Several studies have shown that an electromagnetic field (EMF) can influ- ence both inflammatory processes and repair mechanisms including wound healing on different tissue models. Objectives To elucidate the effect of extremely low frequency EMF (ELF-EMF) on keratinocyte proliferation and production of chemokines [RANTES, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1a and interleukin (IL)-8] in order to evaluate a potential therapeutic use of mag- netic fields. Methods The human keratinocyte cell line HaCaT was exposed at 1 mT, 50 Hz for different lengths of time and compared with unexposed control cells. Cell growth and viability were evaluated at different exposure times by cell count and trypan blue exclusion. Chemokine production and expression were analysed by enzyme- linked immunosorbent assay (ELISA) and by real-time polymerase chain reaction. Total NF-jB p65 was quantified by ELISA. Results Significantly increased growth rates were observed after 48 h of EMF exposure as compared with control cells, while no difference in cell viabilities were detected. Gene expression and release of RANTES, MCP-1, MIP-1a and IL-8 were significantly reduced after 72 h of exposure. NF-jB levels became almost undetectable after only 1 h of EMF exposure, and were inversely correlated with cell density. Conclusions Our results show that ELF-EMF modulates chemokine production and keratinocyte growth through inhibition of the NF-jB signalling pathway and thus may inhibit inflammatory processes. ELF-EMF could represent an additional ther- apeutic approach in the treatment of skin injury.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/133497
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