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Special Senses
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Kenneth A. Schafer, Oliver C. Turner, Richard A. Altschuler
The function, morphology, and pathology of the RPE has been reviewed (Mecklenburg and Schraermeyer 2007; Whiteley and Peiffer 2002). Apical villi of the RPE envelop the photoreceptor outer segments but are separated by the interphotoreceptor matrix. During the disc shedding process, the RPE engulfs and degrades the photoreceptor cell outer segments. Disc shedding may be measured as a function of the RPE (LaVail 1976). Some breakdown products are recycled, but lipofuscin may accumulate as a result of oxidation of polyunsaturated fatty acids as a part of the aging process. Unlike other laboratory animals, lipid bodies normally occur in the RPE of rabbits (Prince 1964).
Effect of hydroxychloroquine or chloroquine and short wavelength light on in vivo retinal function and structure in mouse eyes
Published in Clinical and Experimental Optometry, 2023
Wilson Heriot, Vickie HY Wong, Zheng He, Anh Hoang, Jeremiah KH Lim, Tomoharu Nishimura, Da Zhao, Andrew B Metha, Bang V Bui
The mechanism of CQ and HCQ induced retinal changes is not completely understood. One commonly accepted theory is that toxic accumulation of HCQ/CQ in the RPE hinders lysosomal function.30 HCQ and CQ have high affinity for melanin and accumulate in the uvea and the RPE.31,32 Deposition of HCQ/CQ in the RPE results in increased pH in lysosomes, which inhibits the capacity for lysosomes to fuse with phagosomes, thereby impairing intracellular autophagy and phagocytosis. Impaired phagocytosis and autophagy result in accumulation of photoreceptor discs, other spent organelles, and lipofuscin in the RPE, which ultimately lead to degeneration of the RPE and neuroretina. Even after 2 weeks of HCQ treatment, there was evidence of RPE thickening on SD-OCT in this murine model. RPE dysfunction and reduced outer segment disc shedding would account for the finding of longer photoreceptor outer segments.
Circadian rhythms in diabetic retinopathy: an overview of pathogenesis and investigational drugs
Published in Expert Opinion on Investigational Drugs, 2020
Ashay D. Bhatwadekar, Varun Rameswara
The mammalian retina is about 200 µm thick and contains a varied collection of neuronal cell types comprised mainly of six classes of neurons: rods, cones, horizontal cells, amacrine cells, bipolar cells, and retinal ganglion cells. These neurons exhibit a laminar distribution, further differentiating into layers with different cell types forming the nuclear layers and different synapses forming the plexiform layers [13]. Light is the most potent driver for synchronizing daily activities, and the retina plays an integral role in sensing light via rods, cones, and ipRGCs. In contrast to rods and cones, which are responsible for vision forming, the ipRGCs are non-image forming and have the ability to communicate to the SCN and beyond, affecting several aspects of mammalian health. The mammalian retinal circadian rhythm is independent of the master circadian clock, the SCN. This retinal circadian system plays a vital role in a range of physiological functions of the eye, such as visual processing, changes in corneal thickness and intraocular pressure, disc shedding and phagocytosis, and susceptibility to light-induced photoreceptor damage. Therefore, disruption of the circadian clock in the retina negatively affects eye health.
Does the circadian clock make RPE-mediated ion transport “tick” via SLC12A2 (NKCC1)?
Published in Chronobiology International, 2019
Nemanja Milićević, Angelica Duursma, Anneloor L. M. A. ten Asbroek, Marie-Paule Felder-Schmittbuhl, Arthur A. Bergen
Numerous physiological processes within the mammalian eye show day-night variations, such as: ion channel sensitivity (Ko et al. 2001), melatonin synthesis (Tosini and Menaker 1996), photoreceptor disc shedding (LaVail 1976) and intraocular pressure (Rowland et al. 1981). These daily alterations are driven by light and circadian clocks. On a molecular level, these circadian oscillations are generated by interlocking transcriptional and translational feedback loops comprised of core clock genes: Per1-3, Cry1-2, Bmal1, Rev-erbα-β and Clock (Ko and Takahashi 2006). Many ocular tissues harbor circadian oscillators including the retinal pigment epithelium (RPE) (Baba et al. 2010).