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Janethe D. O. Pena, Olga Agapova, B’Ann T. Gabelt, Leonard A. Levin, Mark J. Lucarelli, Paul L. Kaufman, M. Rosario Hernandez; Increased Elastin Expression in Astrocytes of the Lamina Cribrosa in Response to Elevated Intraocular Pressure. Invest. Ophthalmol. Vis. Sci. 2001;42(10):2303-2314.
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purpose. To determine whether abnormal elastin synthesis in the glaucomatous
optic nerve head and lamina cribrosa is due to elevated intraocular
pressure (IOP) or secondary to axonal injury, monkeys with elevated IOP
and with optic nerve transection were compared .
methods. Unilateral, chronic elevated IOP was induced in 11 rhesus monkeys by
laser scarification of the trabecular meshwork. IOP was monitored
weekly and maintained within 25 to 45 mm Hg for 7 to 36 weeks. In 6
monkeys, unilateral, optic nerve transection was performed, and monkeys
were killed after 4 weeks. Optic nerve damage was assessed by
stereoscopic slit-lamp biomicroscopy and fundus photography and by
confocal scanning laser ophthalmoscopy. The eyes were enucleated and
processed for immunohistochemistry and in situ hybridization and for
electron microscopic immunogold detection of elastin. Axonal loss was
evaluated in cross sections of the optic nerve stained with
results. Compared with normal contralateral controls, the lamina cribrosa of
eyes with elevated IOP exhibited markedly increased elastin and the
presence of elastotic aggregates in the extracellular matrix and
upregulation of elastin mRNA in the astrocytes. In transected eyes,
elastin appeared as fine fibers in the lamina cribrosa, without
elastotic aggregates, and without new synthesis or abnormal deposition
of elastin. At the transected site, new synthesis of elastin was
present in the pia mater but not in astrocytes in the glial scar.
conclusions. This study demonstrates that abnormal elastin synthesis in experimental
glaucomatous optic neuropathy in the monkey is specific to elevated IOP
and not secondary to axonal loss. The mechanisms by which elevated IOP
induces enhanced elastin synthesis in laminar astrocytes are unknown
but differ from those involved in acute axonal injury such as
transection, where inflammation and breakdown of the blood–nerve
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