Introduction Photobiomodulation (PBM) can affect a set of different biological modulators either in vitro or in vivo. It Is known that cellular exposure to low energy light activates a set of biochemical pathways, which modulates the activity of many cellular organelles, influencing cellular homeostasis and functionality of several organs. In this report, we show the effects of PBM on a monocyte/macrophage established tumor cell line (U-937). Methods A NIR-LED device, characterized by an 880 nm-wavelength, has been used as a light source (Tr-Lux, Errevi, Italy). U937 cells (ATCC; Manassas, VA, USA) were grown in RPMI 1640 supplemented with 10% heat-inactivated fetal bovine serum (FBS), 2 mM L-glutamine and 1% Pen-Strep at 37 °C in 5% CO2. The concentration of several cytokines was detected using a Cytofluorimetry FITC-labelled assay and the level of expression of p65 NF-kB and cleaved Caspase-3 by Western blot analysis were analysed. Results This study shows that LED exposure at 880 nm-wavelength activates cell degranulation, beta galactosidase activity and promotes a statistically significant modulation of IL-8 and IL-1β. In all experiments the IL-8 induction was 10 times higher than the basal level. When we tested the LED exposure on U937 cells, in the presence or absence of LPS, surprisingly we observed a slight increase on the release of cytokines in particular regarding IL-8. Additionally, evidences were raised that the well-known pro-inflammatory NF-kB transcription factor and the apoptotic marker, cleaved Caspase-3, were upregulated in response to a proinflammatory biochemical pathway. Conclusions These data, showing that IL-8, is the most induced cytokine after 880 nm LED exposure on U937 cells, strongly attribute a specific role to low energy LED emission in promoting apoptosis, allowing cellular regeneration on target organs. and effecting remodeling process on target cells, including neo-angiogenesis, wound healing and tissue repair mechanisms.
Molecular pathways involved in the regenerative effect induced by photobiomodulation on U937 cell line
MARTINOTTI, Stefano;
2016-01-01
Abstract
Introduction Photobiomodulation (PBM) can affect a set of different biological modulators either in vitro or in vivo. It Is known that cellular exposure to low energy light activates a set of biochemical pathways, which modulates the activity of many cellular organelles, influencing cellular homeostasis and functionality of several organs. In this report, we show the effects of PBM on a monocyte/macrophage established tumor cell line (U-937). Methods A NIR-LED device, characterized by an 880 nm-wavelength, has been used as a light source (Tr-Lux, Errevi, Italy). U937 cells (ATCC; Manassas, VA, USA) were grown in RPMI 1640 supplemented with 10% heat-inactivated fetal bovine serum (FBS), 2 mM L-glutamine and 1% Pen-Strep at 37 °C in 5% CO2. The concentration of several cytokines was detected using a Cytofluorimetry FITC-labelled assay and the level of expression of p65 NF-kB and cleaved Caspase-3 by Western blot analysis were analysed. Results This study shows that LED exposure at 880 nm-wavelength activates cell degranulation, beta galactosidase activity and promotes a statistically significant modulation of IL-8 and IL-1β. In all experiments the IL-8 induction was 10 times higher than the basal level. When we tested the LED exposure on U937 cells, in the presence or absence of LPS, surprisingly we observed a slight increase on the release of cytokines in particular regarding IL-8. Additionally, evidences were raised that the well-known pro-inflammatory NF-kB transcription factor and the apoptotic marker, cleaved Caspase-3, were upregulated in response to a proinflammatory biochemical pathway. Conclusions These data, showing that IL-8, is the most induced cytokine after 880 nm LED exposure on U937 cells, strongly attribute a specific role to low energy LED emission in promoting apoptosis, allowing cellular regeneration on target organs. and effecting remodeling process on target cells, including neo-angiogenesis, wound healing and tissue repair mechanisms.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
