Investigative ophthalmology & visual science · 2001
Increased elastin expression in astrocytes of the lamina cribrosa in response to elevated intraocular pressure.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Pena J D, Agapova O, Gabelt B T, Levin L A, Lucarelli M J, Kaufman P L, Hernandez M R
Аннотация
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 phenylenediamine.
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 barrier occur.
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 phenylenediamine.
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 barrier occur.