Light-emitting-diode induced retinal damage and its wavelength dependency in vivo

AIM： To examine light-emitting-diode（LED）-induced retinal neuronal cell damage and its wavelength-driven pathogenic mechanisms.METHODS： Sprague-Dawley rats were exposed to blue LEDs（460 nm）,green LEDs（530 nm）,and red LEDs（620 nm）.Electroretinography（ERG）,Hematoxylin and eosin（H＆E） staining,transmission electron microscopy（TEM）,terminal deoxynucleotidyl transferase d UTP nick end labeling（TUNEL）,and immunohistochemical（IHC） staining,Western blotting（WB） and the detection of superoxide anion（O2^-·）,hydrogen peroxide（H2O2）,total iron,and ferric（Fe^3＋） levels were applied.RESULTS： ERG results showed the blue LED group induced more functional damage than that of green or red LED groups.H＆E staining,TUNEL,IHC,and TEM revealed apoptosis and necrosis of photoreceptors and RPE,which indicated blue LED also induced more photochemical injury.Free radical production and iron-related molecular marker expressions demonstrated that oxidative stress and ironoverload were associated with retinal injury.WB assays correspondingly showed that defense gene expression was up-regulated after the LED light exposure with a wavelength dependency.CONCLUSION： The study results indicate that LED bluelight exposure poses a great risk of retinal injury in awake,task-oriented rod-dominant animals.The wavelengthdependent effect should be considered carefully when switching to LED lighting applications.

Multi-watt near-infrared light therapy as a neuroregenerative treatment for traumatic brain injury

Infrared light represents a broad spectrum of light with wavelengths from 700 nm to 1 million nm（1,000 microns）.At its shortest wavelengths（referred to as near-infrared）,it merges with the red spectrum of visible light.At the longest end（referred to as far-infrared）,it blends into the range of microwaves.

Correlation between photoreceptor injury-regeneration and behavior in a zebrafish model

Direct exposure to intensive visible light can lead to solar retinopathy, including macular injury. The signs and symptoms include central scotoma, metamorphopsia, and decreased vision. However, there have been few studies examining retinal injury due to intensive light stimulation at the cellular level. Neural network arrangements and gene expression patterns in zebrafish photoreceptors are similar to those observed in humans, and photoreceptor injury in zebrafish can induce stem cell-based cellular regeneration. Therefore, the zebrafish retina is considered a useful model for studying photoreceptor injury in humans. In the current study, the central retinal photoreceptors of zebrafish were selectively ablated by stimulation with high-intensity light. Retinal injury, cell proliferation and regeneration of cones and rods were assessed at 1, 3 and 7 days post lesion with immunohistochemistry and in situ hybridization. Additionally, a light/dark box test was used to assess zebrafish behavior. The results revealed that photoreceptors were regenerated by 7 days after the light-induced injury. However, the regenerated cells showed a disrupted arrangement at the lesion site. During the injury-regeneration process, the zebrafish exhibited reduced locomotor capacity, weakened phototaxis and increased movement angular velocity. These behaviors matched the morphological changes of retinal injury and regeneration in a number of ways. This study demonstrates that the zebrafish retina has a robust capacity for regeneration. Visual impairment and stress responses following high-intensity light stimulation appear to contribute to the alteration of behaviors.

Down-regulation of protein kinase C alpha/ezrin signals in light-induced phagocytic crisis of retinal pigment epithelium cells

AIM： To investigate the roles of PKC-α/ezrin signals in phagocytosis crisis of retinal pigment epithelium（RPE） cells in light damage model. METHODS： Light induced mice RPE injury model was established by continuously irradiating cool white light at different exposure time（0, 4, 8h light intensity： 4.18×10^-6 J/cm^2）. In vitro, human ARPE-19 cells treated with the doses and intensity（1.57×10^-6 J/cm^2） of laser irradiation. Histology analysis was evaluated by hematoxylin and eosin（HE） staining. In vivo RPE phagocytosis was quantified by measuring the accumulation of photoreceptor outer segments in the sub-retinal space. In vitro RPE phagocytosis was assessed by calculating the relative fluorescence intensity of FITC-labeled microspheres in ARPE-19 cells. To further investigate the molecular mechanism, the activation of PKC-α/ezrin signal was evaluated by Western blot in vivo and in vitro.RESULTS： HE staining revealed that the thickness of outer nuclear layer decreased significantly after 4 and 8h light exposure. By immunostaining with rhodopsin, a significant greater accumulation of photoreceptor outer segment was noticed after light injury. In vitro, light injuredRPE cells had less phagocytic activity in a dose dependent manner than that of the normal control（P〈0.01）. Western blot suggested the activation of PKC-α/ezrin signaling was down-regulated in a dose-dependent manner after light exposure. CONCLUSION： Our data suggest that light induced phagocytic crisis of RPE cells may result from the downregulation of PKC-α/ezrin signaling.