Cochlin and glaucoma: A mini-review

Sanjoy K. Bhattacharya, Neal S. Peachey, John W. Crabb

Research output: Contribution to journalShort surveypeer-review

20 Scopus citations

Abstract

Primary open angle glaucoma (POAG) is a leading cause of late onset, progressive, irreversible blindness and, although its etiology is poorly understood, elevated intraocular pressure (IOP) often appears to be a contributory factor. Proteomic and Western analyses of trabecular meshwork (TM) from patients with POAG and age-matched controls originally implicated cochlin as possibly contributing to glaucoma pathogenesis. Cochlin deposits were subsequently detected in glaucomatous but not in control TM and older glaucomatous TM was found to contain higher levels of cochlin and significantly lower amounts of collagen type II. More recently, similar results were reported in DBA/2J mice, which at older ages develop elevated IOP, retinal ganglion cell degeneration, and optic nerve damage. Notably, cochlin was absent in TM from C57BL/6J. CD1, and BALBc/ByJ mice, which do not exhibit elevated IOP or glaucoma. Cochlin was found in the TM of very young DBA/2J mice, prior to elevated IOP, suggesting that over time the protein may contribute to the events leading to increased IOP and optic nerve damage. Here we review these findings and describe how future studies in DBA/2J mice can help resolve whether cochlin plays a causal role in mechanisms of POAG and elevated IOP.

Original languageEnglish (US)
Pages (from-to)605-613
Number of pages9
JournalVisual neuroscience
Volume22
Issue number5
DOIs
StatePublished - Sep 2005
Externally publishedYes

Keywords

  • Cochlin
  • Glaucoma
  • Intraocular pressure
  • Optic nerve damage
  • Trabecular meshwork

ASJC Scopus subject areas

  • Neuroscience(all)

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