China
Africa
Explore chapters and articles related to this topic
Imaging the Living Eye
Published in Margarida M. Barroso, Xavier Intes, In Vivo, 2020
Brian T. Soetikno, Lisa Beckmann, Hao F. Zhang
As shown in Figure 14.1C, the retina is composed of eight distinct layers grouped into the outer and inner retinae. The outer retina consists of photoreceptors and the retinal pigment epithelium (RPE). Photoreceptors are further divided into rod and cone photoreceptors, which are responsible for low-light vision and color perception, respectively. The RPE layer contains various pigments, including melanin, that aid in absorbing irradiating light energy among other physiological roles. In addition, the RPE also transports nutrients between the photoreceptors and the choriocapillaris, participates in the visual cycle, removes shed photoreceptor membranes by phagocytosis, and secretes a variety of growth factors (Strauss, 2005). The inner retina consists of four classes of neurons: ganglion cells, amacrine cells, horizontal cells, and bipolar cells. The combination and connections of these cells form small neuronal networks that amplify, process, and filter information from the photoreceptors (Wassle, 2004). Eventually, the ganglion cell bodies collect the partially processed information, and their axons, which together form the optic nerve, transmit the information to the visual cortex of the brain for further higher-level information processing.
Induced Pluripotent Stem Cells: A Research Tool and a Potential Therapy for RPE-Associated Blinding Eye Diseases
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Ruchi Sharma, Balendu Shekhar Jha, Kapil Bharti
The retinal pigment epithelium (RPE) is a polarized monolayer epithelium located in the back of the eye between the photoreceptors and the choroidal blood supply. The retina/RPE/choroid form a homeostatic unit in the back of the eye, and RPE is critically important for maintaining the health of this homeostatic unit. RPE is also responsible for photoreceptor development, and the formation of photoreceptor outer segments is tightly coupled to the presence of functionally normal RPE in the adjacent layer (Raymond and Jackson, 1995; Bumsted et al., 2001; Adijanto et al., 2009; Nasonkin et al., 2013). Mouse models with incomplete RPE differentiation or with dysfunctional RPE do not develop normal photoreceptor outer segments (Raymond and Jackson, 1995; Bumsted et al., 2001; Nasonkin et al., 2013). In addition to its developmental role in regulating photoreceptor differentiation, RPE maintains several photoreceptor functions by: (a) reisomerization of all-trans-retinal, a by-product of visual cycle in photoreceptors, to 11-cis-retinal components and transporting it back to photoreceptors (von Lintig et al., 2010); (b) phagocytosis of photoreceptor outer segments that are damaged by light-induced photooxidation of proteins and lipids (Mazzoni et al., 2014); (c) maintenance of chemical composition and volume of the subretinal space and the choroid. RPE continuously transports water and CO2 from the subretinal space toward the choroid (Adijanto et al., 2009; Li et al., 2009); and (d) constitutively secretes of cytokines in a polarized fashion toward the retina and the choroid to regulate their development, function, and pathophysiology (Shi et al., 2008). The relevance of RPE and its functions in photoreceptor health is underscored by gene mutations and disease conditions where these functions are compromised. For instance, mutations in the enzyme retinal pigment epithelium-specific protein 65 kDa (RPE65) that causes reisomerization of all-trans-retinal to 11-cis-retinal in the RPE, lead to photoreceptor cell death and a disease called Leber congenital amaurosis (LCA) (Cideciyan, 2010). Similarly, mutations in the cell surface protein MER proto-oncogene tyrosine kinase (MERTK) that affects RPE’s ability to phagocytose photoreceptor outer segments also result in photoreceptor cell death subsequently leading to another form of LCA (den Hollander et al., 2008). Furthermore, in age-related macular degeneration (AMD), one of the main factors leading to choroidal neovascularization and to compromised RPE barrier function is the increased basal VEGF secretion by the RPE (Marneros, 2013).
Multiphoton imaging of the retina
Published in Pablo Artal, Handbook of Visual Optics, 2017
Robin Sharma, Jennifer J. Hunter
The first stages in vision depend on the absorption of a photon of light by a photopigment molecule that is located on the membrane in the photoreceptor outer segment. This begins the phototransduction cascade for generating a photocurrent and the visual (or retinoid) cycle for regenerating photopigment. The visual cycle begins with the photoisomerization of the chromophore 11-cis-retinal (vitamin A) and the release of all-trans-retinal from the photopigment. This is quickly converted into all-trans-retinol through a reaction that uses NADPH (Palczewski et al., 1994). This fluorescent molecule is then moved to the RPE where it is esterified to all-trans-retinyl ester. The retinyl ester may be stored in liposomes known as retinyl-ester storage particles or retinosomes (Golczak et al., 2005; Imanishi et al., 2004a,b). These retinosomes are spread throughout the RPE cell and are highly fluorescent. When needed to regenerate photopigment, 11-cis-retinol is isomerized from the retinyl ester. It is then oxidized into 11-cis-retinal before being transported into the photoreceptor outer segments during what is thought to be the rate limiting step of the visual cycle (Lamb and Pugh, 2006). The chromophore, 11-cis-retinal, binds with rhodopsin or the cone opsins to form the photopigment. The aldehyde form of vitamin A exhibits very little fluorescence compared to the alcohol and ester forms. For detailed reviews of the visual cycle, see (Garwin and Saari, 2000; Lamb and Pugh, 2004; McBee et al., 2001; Palczewski, 2014). In addition to this traditional visual cycle, cone photopigment may be regenerated through an alternate faster pathway involving Müller cells (Mata et al., 2002; Muniz et al., 2007; Wang and Kefalov, 2011, 2009). In this case, 11-cis-retinol is transported from the Müller cells into cone inner segments, which are able to convert it into 11-cis-retinal. Evidence suggests that this conversion is not possible in rods (Ala-Laurila et al., 2009; Jones et al., 1989). As the concentration of retinoids changes with visual stimulation, the intensity of emitted fluorescence will vary accordingly. Disruption of the visual cycle may be measured as a variation in the fluorescence intensity of the photoreceptors or RPE in response to light stimulation. In healthy humans, the recovery of sensitivity when light levels are abruptly reduced (e.g., temporarily reduced vision when walking into a darkened theater) is partly governed by the rate of the visual cycle and is known to become slower with age (Jackson et al., 1999). Many blindness-causing diseases are linked to defects in the visual cycle, such as Stargardt macular degeneration, Leber congenital amaurosis, and retinitis pigmentosa (Palczewski and Baehr, 2005).
Recent advances in imaging technologies for assessment of retinal diseases
Published in Expert Review of Medical Devices, 2020
Taha Soomro, Neil Shah, Magdalena Niestrata-Ortiz, Timothy Yap, Eduardo M. Normando, M. Francesca Cordeiro
In the early 1990s Delori et al. were able to use spectrophotometry and examine excitation and emission spectra of FAF in the retina [51]. This highlighted the predominant source of fluorescence in the retina is lipofuscin, a fluorophore, which is a by-product of the visual cycle which accumulates within the retinal pigment epithelium (RPE) [52].