This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Elevated intraocular pressure (IOP) is an important risk factor for optic nerve damage in glaucoma. The precise pathophysiological mechanism that leads to RGC death in glaucomatous optic nerve damage by elevated IOP remains unknown. Mitochondrial changes have been involved in the pathophysiology of neuronal death and it is reasonable to speculate that they, too, may cause glaucomatous optic neuropathy. Mitochondrial fission is a cellular response to stress that has an important role in neuronal cell death in neurodegenerative diseases. Our goal is to determine whether elevated hydrostatic pressure induces mitochondrial fission and dysfunction in cultured retinal ganglion cells, primary retinal ganglion cells, and in the neurons and astrocytes of optic nerve head in DBA mice, which serve as a model for age-related glaucoma. We will use the advanced imaging capability of electron microscope tomography to investigate the mitochondrial structural perturbations in glaucoma models.
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