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Int. J. Mol. Sci. 2020, 21, 2370 12 of 20 model. It could, therefore, be concluded that too much ROS production causes damage but a moderate amount of ROS is not harmful, sometimes even protective. Consistent with what has been previously reported, the levels ROS staining in BL irradiated eyes were higher in OS than IS [52]. Our results show reduced ROS production in photoreceptor IS and OS upon RL/NIRL irradiation supporting the theory of less cell stress due to reduced intracellular ROS. However, the slight increase of ROS production of RL/NIRL treated compared to non-irradiated photoreceptors might be beneficial in activating NF-kB. As the mitochondrial respiratory chain is the major ROS generation site, large amounts of ROS can be produced based on incomplete oxygen reduction by OXPHOS complexes of mitochondria [55]. We suggest that upon BL damage oxidative phosphorylation is uncoupled, leading to a sensibly reduced ATP synthesis and enhanced ROS production [52]. The detected extramitochondrial complexes might be an additional source for the production of free radicals besides the detected NADPH oxidases in OS [30]. The described membrane opening during mitochondrial related apoptosis pathway can also uncouple oxidative phosphorylation causing inhibition of ATP production and incomplete oxygen reduction shunted into ROS production [56]. Consistent with the modulatory effect from RL/NIRL stimulation on ROS production, the amount of detected lipid peroxidation in photoreceptors was reduced. In addition to the already reported 670 nm RL triggered reduction of 4HNE in photoreceptor OS and in the optic nerve, we could show a reduced HEL expression [4,18]. As mentioned, since most PBM studies are limited to 670 nm, we provide data about 810 nm NIRL exposure on 4HNE and HEL. We speculate that RL inhibits lipid peroxidation because of increased Bcl-2 expression. Bcl-2 overexpression leads to the complete suppression of lipid peroxidation [57]. RL/NIRL treatment modulation of ROS production and Nox4 expression consequent to BL irradiation was especially evident in isolated OS. Finally, the RL/NIRL mediated neuroprotective impact on ROS production and lipid peroxidation on photoreceptors leading to less oxidative cell stress. One major point in our study was the analysis of regulatory factors that might mediate changes in oxidative stress levels and mitochondrial function upon BL and especially NIRL/RL treatment. Our study revealed 22 genes with significant expression changes for C vs. BL, seven genes for BL vs. BL+NIRL 810 nm and nine genes for BL vs. BL+RL 670 nm. A recently published study identified gene expression changes in photoreceptors of Drosophila melanogaster [58]. The expression of 44 genes altered one day after BL expression and 568 genes 6 days after BL expression. These genes are part of stress response pathways, calcium influx and ion transport. This study, as well as our study, identified different DEGs, but both include genes with neuroprotective functions. Differences may have various causes, for example, the chosen species and BL exposure settings (duration, wavelength). Similar to the drosophila study, it might be possible that the small number of altered genes could increase after longer cultivation time or BL, RL and NIRL exposure time. Considering the mentioned study, we suggest that the identified DEGs are limited to the precise experimental conditions. Another possible explanation for a small number of DEGs considers that BL, RL and NIRL affect predominantly the protein level of murine photoreceptors. The most common assumptions of RL/NIRL mediated alterations in genes include transcription factors such as NF-κB, RANKL, RUNX2 and HIF1α [59]. We were able to outline the changes of RL/NIRL on differential gene expression and identified genes that have potential neuroprotective functions. Our study showed that these significantly altered genes include α-crystallins, pointing to the rescued mitochondrial function. We demonstrate inhibited expression of α-crystallins genes cryaa and cryab after BL and upregulation upon RL stimulation. α-crystallins have already been described to be implicated in several cellular processes, including survival and cell death pathways, oxidative stress and neuroprotection. Our study provides evidence that PBM regulates the NF-κB pathway, which improves cell survival, via crystallins based on the recent discovery of NF-κB as a target of αB-crystallin [60]. Moreover, reported functions of α-crystallin in the retina and RPE indicate a role in mitochondria in an anti-apoptotic manner. The αB-crystallin is postulated to interact directly with the pro-apoptotic members Bax and Bcl-Xs suppressing mitochondrial apoptosis [36]. A deficiency of αB-crystallinPDF Image | Photobiomodulation Mediates Neuroprotection against Retinal
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