Articles by Sauparnika Vijay in JoVE
Experimental Glaucoma Induced by Ocular Injection of Magnetic Microspheres Shannon Bunker1, Joanna Holeniewska1, Sauparnika Vijay2, Annegret Dahlmann-Noor2,3, Peng Khaw2,4, Yin-Shan Ng5, David Shima1,6, Richard Foxton1 1Ocular Biology and Therapeutics, University College London Institute of Ophthalmology, 2University College London Institue of Ophthalmology, 3Moorfields Eye Hospital, 4NIHR Biomedical Research Centre, Moorfields Eye Hospital, 5Schepens Eye Research Institute, Harvard Medical School, 6Hoffman-La Roche We present a method for inducing elevated intraocular pressure (IOP), by injecting magnetic microspheres into the rat eye, to model glaucoma. This leads to strong pressure rises, and extensive neuronal death. This protocol is easy to perform, does not require repeat injections, and produces stable long-lasting IOP rises.
Other articles by Sauparnika Vijay on PubMed
Current Approaches and Future Prospects for Stem Cell Rescue and Regeneration of the Retina and Optic Nerve Canadian Journal of Ophthalmology. Journal Canadien D'ophtalmologie. Aug, 2010 | Pubmed ID: 20648090 The 3 most common causes of visual impairment and legal blindness in developed countries (age-related macular degeneration, glaucoma, and diabetic retinopathy) share 1 end point: the loss of neural cells of the eye. Although recent treatment advances can slow down the progression of these conditions, many individuals still suffer irreversible loss of vision. Research is aimed at developing new treatment strategies to rescue damaged photoreceptors and retinal ganglion cells (RGC) and to replace lost cells by transplant. The neuroprotective and regenerative potential of stem and progenitor cells from a variety of sources has been explored in models of retinal disease and ganglion cell loss. Continuous intraocular delivery of neurotrophic factors via stem cells (SC) slows down photoreceptor cells and RGC loss in experimental models. Following intraocular transplantation, SC are capable of expressing proteins and of developing a morphology characteristic of photoreceptors or RGC. Recently, recovery of vision has been achieved for the first time in a rodent model of retinal dystrophy, using embryonic SC differentiated into photoreceptors prior to transplant. This indicates that clinically significant synapse formation and acquisition of the functional properties of retinal neurons, and restoration of vision, are distinct future possibilities.
VEGF-A is Necessary and Sufficient for Retinal Neuroprotection in Models of Experimental Glaucoma The American Journal of Pathology. Apr, 2013 | Pubmed ID: 23416159 Vascular endothelial growth factor A (VEGF-A) is a validated therapeutic target in several angiogenic- and vascular permeability-related pathological conditions, including certain cancers and potentially blinding diseases, such as age-related macular degeneration and diabetic retinopathy. We and others have shown that VEGF-A also plays an important role in neuronal development and neuroprotection, including in the neural retina. Antagonism of VEGF-A function might therefore present a risk to neuronal survival as a significant adverse effect. Herein, we demonstrate that VEGF-A acts directly on retinal ganglion cells (RGCs) to promote survival. VEGF receptor-2 signaling via the phosphoinositide-3-kinase/Akt pathway was required for the survival response in isolated RGCs. These results were confirmed in animal models of staurosporine-induced RGC death and experimental hypertensive glaucoma. Importantly, we observed that VEGF-A blockade significantly exacerbated neuronal cell death in the hypertensive glaucoma model. Our findings highlight the need to better define the risks associated with use of VEGF-A antagonists in the ocular setting.