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Hannah Fisher, Gopika Senthikumar, Janis T Eells, Elizabeth S Liedhegner; 670 nm Photobiomodulation Modifies NFκB Signaling in an in vitro Model of Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5223.
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© ARVO (1962-2015); The Authors (2016-present)
Diabetic retinopathy (DR) is the most common complication of diabetes mellitus and a leading cause of blindness. The pathophysiology of DR is complicated, involving inflammation, oxidative stress and vascular degeneration. Diabetes-induced oxidative stress leads to activation of nuclear factor κ B (NFκB) resulting in excess production of vascular endothelial growth factor (VEGF) and intracellular adhesion molecule-1 (ICAM-1), proteins involved in vascular development and immune dysregulation. Current treatments for diabetic retinopathy antagonize the actions of VEGF and reduce vascular growth. These treatments are invasive and frequently ineffective. Irradiation with far-red to NIR light (photobiomodulation, [PBM]) has been shown to non-invasively attenuate oxidative stress and inflammation in many disease states. We hypothesize that 670 nm PBM will reduce the activity of NFκB and attenuate the production of VEGF and ICAM-1 in an in vitro model of DR.
Experiments were conducted in cultured retinal Müller glial cells. Müller glial cells have been shown to play a primary role in the progression of DR due to a shift in their physiology from an anti-inflammatory to a pro-inflammatory state. Müller cells were grown in normal (5 mM) or high (25 mM) glucose conditions to simulate normoglycemia and hyperglycemia. Cultures were treated with 670 nm light emitting diode (LED) (180 seconds at 25 mW/cm2 ; 4.5 J/cm2) or no light (sham) for 3 or 5 days. NFκB activity, VEGF release and ICAM-1 concentrations were measured.
Müller cells grown in high glucose exhibited significant increases in NFκB activity (p < 0.001) and ICAM-1 concentrations (p < 0.0001), consistent with a pro-inflammatory state. In contrast, treatment of cells with 670nm light reduced NFκB gene transcription and downstream protein concentration of ICAM-1 to values comparable to those measured under normoglycemic conditions.
These data support our hypothesis and suggest that activation of NFκB is a key feature of the Müller glial cell response to hyperglycemia. They further show that treatment with 670 nm LED attenuates the NFκB signaling pathway and has the potential to be a valuable therapeutic approach for the treatment of DR.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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