- Assistant Professor of Research, Deptartment of Ophthalmology, University of Oklahoma Health Sciences Center (OUHSC)
- Systems Manager, NEI/DMEI Cellular Imaging Core Facility
- Cerium oxide nanoparticles as antioxidants in preserving vision using rodent retinal degeneration models
- Role of microglia in retinal neovascularization and retinal degeneration
- PhD, Biology, University of Virginia, Charlottesville, VA
- Postdoctoral Training, Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA
- Postdoctoral Training, Dept. of Surgery, Div. of Anatomy, University of California, San Diego, San Diego, CA
Irrespective of causes, many blinding eye diseases exhibit hallmarks of oxidative stress. Oxidative stress or damage results from the inability of cells to detoxify excess reactive compounds such as reactive oxygen species (ROS) and reactive nitrogen species (RNS). Oxidative stress leads to cellular dysfunction and ultimately cell death. It is a common upstream node shared in blinding eye diseases such as inherited retinal degeneration, age-related macular degeneration (AMD) and diabetic retinopathy (DR).
Previously we discovered that cerium oxide nanoparticles (nanoceria: 3-20 nm in size) possess antioxidant activities in vitro, more specifically, they can neutralize ROS. We later demonstrated that administration of nanoceria in the vitreous can reduce oxidative stress in the retina and protect against light-induced retinal degeneration. These nanoparticles have catalytic activities that mimic superoxide dismutase and catalase (endogenous enzymes to neutralize ROS) in vitro. Because of their chemical and physical properties, these nanoparticles can regenerate their redox activities, and therefore may not require repetitive dosing as is common in administration of dietary antioxidants. Nanoceria may become the 21st century antioxidant of choice to prevent cellular oxidative stress.
If elevated level of ROS causes cell death, we hypothesize that removal of excess ROS can protect cells from dying, thus maintaining cell function. We are using several rodent retinal degeneration models to test this hypothesis. In addition, I am interested in studying how the immune system, specifically retinal microglia, modulates the pathogenesis of degenerative retinal diseases. (These projects are conducted in collaboration with Dr James McGinnis.)
Wong, L.L., Hirst, S.M., Pye, Q.N., Reilly, C.M., Seal, S., McGinnis, J.F. 2013. Catalytic Nanoceria are Preferentially Retained in the Rat Retina and are not Cytotoxic after Intravitreal Injection. PLoS ONE 8(3): e58431. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0058431
Zhou, X., Wong, L.L. (co-first author), Karakoti, A.S., Seal, S., and McGinnis, J.F. 2011. Nanoceria Inhibit the Development and Promote the Regression of Pathologic Retinal Neovascularization in the Vldlr knockout mouse. PLoS ONE 6 (2): e16733. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016733
Kong, L., Cai, X., (co-first author), Zhou, X., Wong, L.L., Karakoti, A.S., Seal, S., and McGinnis, J.F. 2011. Nanoceria extend photoreceptor cell lifespan in tubby mice by modulation of apoptosis/survival signaling pathways. Neurobiology of Disease 42: 514-523. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411120/
Wong, L.L. and Rapaport, D.H. 2009. Defining Retinal Progenitor Cell Competence in Xenopus laevis by Clonal Analysis. Development 136:1707-1715. DOI: 10.1242/dev.027607. (Cover Photo for May 15, 2009, Volume 136, Issue 10) http://dev.biologists.org/content/vol136/issue10/cover.shtml
Full CV can be accessed here.