Abstract
Many studies suggest that far-infrared (FIR) therapy can reduce the frequency of some vascular-related diseases. The non-thermal effect of FIR was recently found to play a role in the long-term protective effect on vascular function, but its molecular mechanism is still unknown. In the present study, we evaluated the biological effect of FIR on vascular endothelial growth factor (VEGF)-induced proliferation in human umbilical vein endothelial cells (HUVECs). We found that FIR ranging 3∼10 µm significantly inhibited VEGF-induced proliferation in HUVECs. According to intensity and time course analyses, the inhibitory effect of FIR peaked at an effective intensity of 0.13 mW/cm2 at 30 min. On the other hand, a thermal effect did not inhibit VEGF-induced proliferation in HUVECs. FIR exposure also inhibited the VEGF-induced phosphorylation of extracellular signal-regulated kinases in HUVECs. FIR exposure further induced the phosphorylation of endothelial nitric oxide (NO) synthase (eNOS) and NO generation in VEGF-treated HUVECs. Both VEGF-induced NO and reactive oxygen species generation was involved in the inhibitory effect of FIR. Nitrotyrosine formation significantly increased in HUVECs treated with VEGF and FIR together. Inhibition of phosphoinositide 3-kinase (PI3K) by wortmannin abolished the FIR-induced phosphorylation of eNOS and Akt in HUVECs. FIR exposure upregulated the expression of PI3K p85 at the transcriptional level. We further found that FIR exposure induced the nuclear translocation of promyelocytic leukemia zinc finger protein (PLZF) in HUVECs. This induction was independent of a thermal effect. The small interfering RNA transfection of PLZF blocked FIR-increased PI3K levels and the inhibitory effect of FIR. These data suggest that FIR induces the nuclear translocation of PLZF which inhibits VEGF-induced proliferation in HUVECs.
Highlights
Infrared radiation is invisible electromagnetic radiation, the wavelength of which is longer than that of visible light
Vascular endothelial growth factor (VEGF) is induced by hemodialysis graft placement, and increases other mediators to cause the development of venous stenosis [16]
We found that a non-thermal effect of FIR induced translocation of the transcription factor, promyelocytic leukemia zinc finger (PLZF) protein, to nuclei, and inhibited VEGF-induced proliferation in human umbilical vein endothelial cells (HUVECs) via the phosphoinositide 3-kinase/Akt signaling pathway
Summary
Infrared radiation is invisible electromagnetic radiation, the wavelength of which is longer than that of visible light. FIR therapy has the potential to improve endothelial function and reduce the frequency of some vascular-related diseases [1,2,3,4,5]. That study revealed that the nonthermal effects of FIR played a role in the long-term protective effect on vascular function. A histological evaluation revealed that endothelial and fibromuscular hyperplasia is the leading cause of venous stenosis [7,8,9]. Intimal hyperplasia causes AVF intimal thickening with a large number of endothelial cells and a large amount of myofibroblast proliferation [9]. Vascular endothelial growth factor (VEGF) is induced by hemodialysis graft placement, and increases other mediators to cause the development of venous stenosis [16]. The influence of FIR on the function of VEGF is a critical problem in studying the biological activities of FIR on vascular function
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