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Optic nerve head extracellular matrix in primary optic atrophy and experimental glaucoma
J C Morrison1, M E Dorman-Pease, G R Dunkelberger
1Department of Ophthalmology, Oregon Health Sciences University, Portland.
Archives of Ophthalmology (Chicago, Ill. : 1960)
|July 1, 1990
Summary
Glaucoma causes collagen buildup in the optic nerve head's lamina cribrosa, potentially altering its function. This extracellular matrix deposition appears specific to elevated intraocular pressure.
Area of Science:
- Ophthalmology
- Neuroscience
- Biochemistry
Background:
- Glaucoma is a leading cause of irreversible blindness.
- Optic nerve head structure and extracellular matrix composition are crucial for vision.
- Understanding biochemical changes in the lamina cribrosa is vital for glaucoma research.
Purpose of the Study:
- To investigate the extracellular matrix changes in the lamina cribrosa of cynomolgus monkeys with experimental glaucoma.
- To differentiate matrix deposition in glaucomatous optic neuropathy from that in optic nerve transection.
Main Methods:
- Unilateral glaucomatous optic neuropathy and optic nerve transections were induced in cynomolgus monkeys.
- Optic nerve heads were analyzed using light and electron microscopic immunohistochemistry.
- Antibodies against collagen types I, III, IV, and elastin were employed.
Main Results:
- Glaucomatous optic nerve heads showed increased collagen type IV along lamina cribrosa beam margins, indicative of basement membrane material accumulation.
- Material within laminar beam pores, positive for collagen types I, III, and IV (but not elastin), was observed in glaucoma.
- Optic nerve transection led to increased collagen type IV on beam margins due solely to astrocyte basement membranes, without extracellular matrix deposition in pores.
Conclusions:
- Elevated intraocular pressure in glaucoma selectively induces extracellular matrix deposition within the lamina cribrosa pores.
- These biochemical alterations in the lamina cribrosa may impact its biomechanical properties and function in glaucoma patients.
- The findings highlight a specific matrix response to glaucomatous damage, distinct from physical nerve injury.