Photobiomodulation with 670 nm light ameliorates retinal

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Photobiomodulation with 670 nm light ameliorates retinal ( photobiomodulation-with-670-nm-light-ameliorates-retinal )

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ACCEPTED MANUSCRIPT primary Müller cells with photo-oxidative damaged-661W cells did not have a significant effect on Müller cell death (Figure 2D), survival (MTT, Figure 2C), and their ability to produce ATP (Figure 2B). Treatment with 670nm light had no significant effect on these factors (Figure 2B-D). When assessing activation of Müller cells, we found that expression of Gfap, a marker of gliosis, was significantly down-regulated in 670nm-treated Müller cells compared to non-treated stressed cells (P<0.05, Figure 2E). Rlbp1 has been linked with the maintenance of normal metabolic homeostasis in the retina. There was a significant reduction in Rlbp1 expression in stressed Müller cells (Figure 2F). Treatment with 670nm prevented this loss of expression in stressed Müller cells (P<0.05, Figure 2F). To further confirm whether 670nm light influences the function of Müller cells in PD, the neuroprotective effect of Müller cells on 661W photoreceptor cells was measured. In the absence of Müller cells, PD increased cell death (Figure 2I), reduced viability (MTT, Figure 2H) and reduced ATP production (Figure 2G) in 661W cells, compared to non-damaged 661W cells. When co-cultured with Müller cells, 661W cells had elevated levels of ATP and MTT and a reduced level of cell death following PD, compared to control 661W cells (P<0.05). Co-culture with Müller cells treated with 670nm light resulted in increased cell survival and ATP production of 661W cells, as well as reduced cell death. However, these changes were not significantly different from those co-cultured with non-treated Müller cells (Figure 2G-I). Co-culture with Müller cells, treated or un-treated with 670nm, did not alter viability or death of control (non-PD) 661W cells (Figure 2G-I). 3.3 670nm light suppressed oxidative stress and inflammation in Müller cells following PD A key feature of retinal degenerations is the increased production of free radicals and oxidative stress (Nita and Grzybowski, 2016). We examined the gene expression levels of 13 ACCEPTED MANUSCRIPT

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