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M. Rosario Hernandez, D.D.S. [NEI Strategic Planning]

M. Rosario Hernandez, D.D.S.


Dr. M. Rosario Hernandez joined the Department of Ophthalmology and Visual Sciences at Washington University as Associate Professor with tenure in October of 1995. She was granted a joint appointment as Associate Professor in the Department of Anatomy and Neurobiology at that time. She is now a Professor with tenure in Department of Ophthalmology.

The work of Dr. M. Rosario Hernandez introduced cellular and molecular biology to the study of the optic nerve head in glaucoma. Before she began research in this area, passive compression of the connective tissues of the lamina cribrosa was thought to be the cause of axon degeneration in the optic nerve.

For the first time Dr. Hernandez proposed that the remodeling of the optic nerve head in glaucoma was the consequence of abnormal cellular activities that changed irreversibly the natural environment of the axons of the retinal ganglion cells. Her earlier work demonstrated the intricate molecular structure of the extracellular matrix of the lamina cribrosa and how this structure changes with age and in glaucoma. She reasoned that the changes in the structure of the lamina cribrosa required synthesis and degradation of extracellular matrix and she demonstrated that the cells responsible for these changes in ECM are the astrocytes, the major cell population of the optic nerve head.

Her laboratory work demonstrates a broad multidisciplinary approach. Her initial work was based on morphological techniques applied to human tissues, followed by molecular biology and biochemistry. Dr. Hernandez was the first to isolate and culture astrocytes and lamina cribrosa cells from human eyes and use the cells for studies of the effects of pressure in various cellular parameters. She has incorporated to her research the monkey model of glaucoma and of optic nerve transection to complement her observations in ex-vivo human optic nerve heads and in vitro models of biomechanical stress and hypoxia. These monkey studies will allow her to determine the role of elevated intraocular pressure in glaucoma and to differentiate glaucomatous and non-glaucomatous retinal ganglion cell loss.

Her current studies seek to demonstrate a primary or a secondary role of reactive astrocytes in glaucoma; to determine whether astrocytes are partly responsible for suppressing axon regeneration or for creating an inhospitable environment for healthy axons; and to determine whether astrocytes isolate or expand areas of neural damage.

Dr. Hernandez will continue to make significant contributions and to lead the field of glaucoma basic research. Many laboratories are working now in this field and the progress in understanding glaucomatous neuropathy has been significant in the last decade. As a member of the National Eye Advisory Council of NIH and through her many interactions with other scientists, Dr. Hernandez is actively seeking expanding the breath of glaucoma research to include neurobiology and neuroprotection as major targets of future research.

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