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Photobiomodulation for retinal diseases untreated control. This was the first documented demonstration of "laser biostimulation" [6]. Ever since, the study and application of FR/NIR light had been of sustained interest in the medical community (recently reviewed by Chung [8], Rojas and Gonzalez-Lima[9], and Peplow [10]). Over the years, the number of conditions amenable to PBM has greatly increased and their diversity is truly amazing, with the majority having been explored in both animal models and human patients. These range from wound healing, including diabetic ulcers [10-13] to pain control for neurologic neck pain[14] and pain from chronic joint disorders[15] to promotion of the regeneration and functional recovery of tissues with poor healing potential such as injured peripheral [16-17] and optical nerves [9,18], recovery following stroke [19] and other central nervous system damage such as traumatic brain injury [20]. Further, there are a number of applications of PBM to treat retinal disorders, which are the focus of this review and include AMD [ 21 ] , diabetic retinopathy [22], and amblyopia [23], among many others. Although initially it was believed that the light used in PBM had to be coherent and polarized like light produced by the He-Ne laser, these properties are no longer considered essential such that devices containing LED arrays are now widely used in photo-medicine at only a fraction of the cost for a laser[1]. Mechanisms of Action of Photobiomodulation PBM is very different from the conventional use of photon energy in laser medicine where heating and burning are the prevailing mechanisms of action. Instead of relying on thermal activity, this new light therapy approach exploits the photochemical conversion potential of low-intensity FR/NIR (630-1000 nm) light. The first insights into the mechanism of PBM came from studies in the late 1980s and 1990s that implicated mitochondria as the subcellular targets of FR/NIR[24-27]. It was proposed by Karu [28] that cytochrome C oxidase inside mitochondria serves as the primary photoacceptor. Cytochrome C oxidase is the enzyme that catalyzes the transfer of electrons from cytochrome C to molecular oxygen-the final step in the mitochondrial respiratory chain and essential for the sustained availability of energy inside cells. Further studies of the action spectrum of the FR/NIR light (defined as the biological response as a function of wavelength) also pointed towards cytochrome C oxidase as the main photoacceptor mediator[29-30]. Research in cell culture using HeLa cells [30-31], and primary neurons [32], demonstrated directly that PBM enhances the activity of cytochrome C oxidase. For instance, Wong-Riley [32] showed that 670 nm light completely reverses the ability of tetrodotoxin, which is a sodium channel blocker capable of indirect down-regulation of cytochrome C oxidase, to diminish this enzyme's activity in primary cultured neuronal cells. Also, PBM competed with potassium cyanide-an irreversible inhibitor of cytochrome C oxidase such that PBM's effectiveness to protect neurons from dying decreased with the increase of the potassium cyanide concentration. The hypothesis of cytochrome C oxidase being the primary target and effector of PBM is further supported by Eells 's [33] discovery that NIR light reverses the inhibitory and toxic effect of formic acid (the active metabolite in methanol intoxication), on mitochondrial cytochrome C oxidase in rat retinas, resulting in improved vision outcomes. The stimulation of cytochrome C oxidase by FR/NIR light is believed to lead to an increase in the energy production by mitochondria, increase in the metabolic rate, in cell proliferation and migration[6,34]. Further, studies using retinas from diabetic rats demonstrated that PBM leads to decrease in diabetes-induced inflammation or retinal vessels [35]. A cDNA microarray analysis of gene expression profiles in human fibroblast cells irradiated with red light showed that PBM causes marked changes in gene expression, including an upregulation in the proteins that comprise the mitochondrial respiratory chain and anti-oxidant genes[36]. At the same time, PBM was shown to cause a downregulation of genes implicated in apoptosis and the stress response. PBM might also function by increasing the bioavailability of nitric oxide (NO) by prompting its release from intracellular stores such as heme-containing proteins [37-38]. Accordingly, absorption measurements from HeLa cells carried out by Karu [30] demonstrated that PBM leads to NO photo-dissociation from cytochrome C oxidase's heme 3A under normoxic conditions. Since NO functions as an inhibitor of the mitochondrial respiration, its dissociation from cytochrome C oxidase would restore mitochondria's oxygen consumption, which in turn should increase energy production and thus boost cellular metabolism. It is also conceivable, as pointed out by Poyton and Ball [39] in their review, that the dissociated NO could function both as a signal for hypoxia inside the cell and extracellularly where NO diffuses out of the cell and can function as a vasodilator and/or lead to potential additional and still-to-be-discovered downstream effects. However, it is necessary to mention that another study carried out by Tang [35] failed to demonstrate a link to NO as there was no change in the NO concentration in cultured retinal cell lines (RGC5 and 661W) after PBM treatment. Nor was the beneficial effect of PBM in cell culture, under high-glucose stress conditions, diminished by the NO scavenger carboxy-PTIO, indicating an NO-independent mode of action for PBM. Of course, the main caveat to the Karu [30] and Tang [35] studies is that they did not use the same cell line and experimental conditions. 146PDF Image | Photobiomodulation for the treatment of retinal diseases
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