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Editors Selection IGR 8-2

Basic Research - Outflow: Aqueous outflow resistance

Comment by Michael Fautsch on:

46439 Segmental versican expression in the trabecular meshwork and involvement in outflow facility, Keller KE; Bradley JM; Vranka JA et al., Investigative Ophthalmology and Visual Science, 2011; 52: 5049-5057

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In 1873, Dr. Theodore Leber postulated that in the glaucomatous eye, elevated IOP was the result of increased outflow resistance to aqueous humor drainage in the anterior chamber of the eye. More than 130 years later, the mechanisms of outflow resistance in normal and glaucomatous eyes still remain unknown.

The mechanisms of outflow resistance in normal and glaucomatous eyes still remain unknown

While it is widely accepted that the likely site of outflow resistance resides in the interface of the juxtacanalicular region of the trabecular meshwork and the inner wall of Schlemm's canal, identification of the regulatory mechanisms within this area have been elusive. Identifying the molecular components involved in outflow facility modulation is crucial to understanding how outflow resistance is different between normal and glaucomatous eyes. Evidence supporting a role for proteoglycans, specifically versican as a molecule involved in outflow resistance continues to mount. Keller et al. (1160) report that distribution of versican in the trabecular meshwork is inversely proportional to the fluid flow pathway: regions of low fluid flow have high concentrations of versican while high fluid flow regions have considerably lower versican levels.

Disruption of versican may alter the extracellular matrix organization leading to alterations in fluid movement through the trabecular meshwork

RNAi silencing of N-acetylgalactosaminyltransferase-1, an enzyme that Disruption of versican may alter the extracellular matrix organization leading to alterations in fluid movement through the trabecular meshwork catalyzes the chondroitin sulfate glycosaminoglycan biosynthesis, increased outflow facility in human and porcine anterior segment culture. Interestingly, addition of lentivirus vectors containing versican shRNA-silencing cassettes showed decreased outflow facility in human anterior segments but increased outflow facility in porcine eyes suggesting species specific roles. This is an excellent study with plausible discussion as to the importance of versican interaction with other extracellular matrix molecules, particularly elastin and hyaluronic acid. Disruption of versican may alter the extracellular matrix organization leading to alterations in fluid movement through flow channels in the trabecular meshwork. Additional experimentation is required to determine the extent to which this finding is important in maintaining normal outflow resistance and whether or not differences are seen in the glaucomatous eye.

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