China
Africa
Explore chapters and articles related to this topic
An overview of human pluripotent stem cell applications for the understanding and treatment of blindness
Published in John Ravenscroft, The Routledge Handbook of Visual Impairment, 2019
Louise A. Rooney, Duncan E. Crombie, Grace E. Lidgerwood, Maciej Daniszewski, Alice Pébay
The trabecular meshwork is a small area of cells surrounded by extracellular matrix, located at the base of the cornea, close to the ciliary body. Functioning as the drainage system of the eye, the trabecular meshwork actively redistributes fluid from the anterior chamber of the eye to Schlemm’s canal to maintain intraocular pressure. Additionally, the trabecular meshwork phagocytoses debris, an important feature of the maintenance of healthy aqueous humor and its clearance system. If the trabecular meshwork is inoperable or poorly functioning and regular homeostatic regulation is lost, intraocular pressure rises, which can result in damage to the optic nerve. Therefore, defective functionality of the trabecular meshwork is thought to result in open-angle glaucoma, the most common form of glaucoma. Ding et al. (2014) co-cultured mouse iPSCs with immortalised human trabecular meshwork cells. This technique induces distinct morphological changes and generates iPSC-trabecular meshwork cells that resemble trabecular meshwork cells as described in the literature. Importantly, these cells also exhibit phagocytic functionality, a key feature of trabecular meshwork. hPSCs have been differentiated to trabecular meshwork-like cells by generation of embryoid bodies on trabecular meshwork extracellular matrix in a medium conditioned with meshwork (Abu-Hassan et al., 2015). Trabecular meshwork cells have been then transplanted into animal models of glaucoma, effectively restoring intraocular pressure and improving aqueous humor outflow facility (Abu-Hassan et al., 2015; Zhu et al., 2016; Zhu et al., 2017).
Glaucoma
Published in Mary E. Shaw, Agnes Lee, Ophthalmic Nursing, 2018
Viscocanalostomy. Canulate the Schlemm’s canal, on order to improve the aqueous outflow without going right into the eye, a possible lower risk to the eye than a trabeculectomy, but does not work quite as well in lowering the IOP. This is not a common procedure at the moment in the United Kingdom.
Answers
Published in Calver Pang, Ibraz Hussain, John Mayberry, Pre-Clinical Medicine, 2017
Calver Pang, Ibraz Hussain, John Mayberry
Aqueous humour is produced by the ciliary body. (1) It first drains through the posterior chamber to enter the anterior chamber. (1) Aqueous humour then exits the eye through the trabecular meshwork into Schlemm’s canal (1)
Honeycomb ensemble of corneal epithelium
Published in Clinical and Experimental Optometry, 2023
Karthikeyan Mahalingam, Shivani Joshi, Murugesan Vanathi, Viney Gupta, Shikha Gupta
Netarsudil is known to cause corneal epithelial reticular oedema within few days to weeks after initiation of the treatment.7–10 High intraocular pressure can trigger both corneal oedema and collapse of Schlemm’s canal.11,12Figure 2 differentiates the netarsudil-induced epithelial oedema (Figure 2A) from the high intraocular pressure-induced corneal oedema (Figure 2A). Netarsudil pushes posterior stromal fluid into anterior chamber by increasing efflux through endothelial pumps and possibly simultaneously pushes anterior stromal fluid into epithelium due to increased permeability of tight junctions.9 Altered epithelial intercellular junctions could have prevented fluid percolation and evaporation and a collapsed Schlemm’s canal, further preventing drainage of anterior corneal fluid through conventional aqueous outflow pathways culminating in epithelial oedema.9 Lowering of intraocular pressure can increase the cross-sectional area of Schlemm’s canal.13 In this patient, discontinuation of netarsudil in conjunction with lowering of intraocular pressure (thus opening Schlemm’s canal) helped resolve epithelial oedema.
Anterior Segment Optical Coherence Tomography in Pediatric Ocular Pathology: Imaging Study of 115 eyes
Published in Expert Review of Medical Devices, 2023
The anterior chamber configuration can be assessed with the wide radial scan and the full range radial scan. Cells in uveitis can be clearly observed, as can emulsified silicon oil, but these cannot be distinguished on images (Figure 3a and j). Narrowing of the angle was observed in 15 (13%) of the eyes, with mostly trauma but also tumors and ectopia lentis. Detailed AC angle evaluation was done in all glaucoma cases, and all of the JOAG cases [14 (12.2%)] had a wide-open angle, and abnormal angle tissue was observed in one eye only, which was not visible on gonioscopy (Figure 3i). The Schlemm’s canal was visible in all cases of JOAG and secondary steroid-induced glaucoma. NVG secondary to retinoblastoma had a narrow angle and anterior displacement of the iris and lens diaphragm.
Glaucoma – ‘A Stiff Eye in a Stiff Body’
Published in Current Eye Research, 2023
Sarah Powell, Mustapha Irnaten, Colm O’Brien
Vahabikashi et al.26 demonstrated Schlemm’s canal (SC) tissue was stiffer in glaucomatous eyes versus those of normal controls, particularly within 1 µm of the inner wall using AFM.26 Furthermore, glaucoma eyes had higher outflow resistance than normal subjects, resulting in decreased AH flow rates through the eye. These findings support the hypothesis that outflow pathway structures undergo biophysical and biomechanical alterations in glaucoma. Similarly, Overby et al.27reported an increase in the cytoskeletal stiffness of SC in glaucomatous eyes, thus contributing to the increase in the outflow resistance characteristically evident in glaucoma pathogenesis.27 This study highlights the mechanosensitive potential of endothelial SC cells that respond to an increase in mechanical strain. This warrants investigation as a potential therapeutic target for glaucoma management in the future. Moreover, Kelly28 et al showed that glaucomatous SC endothelial cells behave differently to normal SC endothelial cells, displaying a fibrotic phenotype characterized by the overexpression of pro-fibrotic ECM genes αlpha smooth muscle actin (αSMA), collagen 1A1 (COL1A1) and fibronectin, as well as transforming growth factor β 2 (TGFβ-2).28