May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Accelerated Cataract Formation in Aquaporin–1 Deficiency in Experiments Models of Cataractogenesis
Author Affiliations & Notes
  • J. Ruiz–Ederra
    Medicine & Physiology, UCSF, San Francisco, CA
  • A.S. Verkman
    Medicine & Physiology, UCSF, San Francisco, CA
  • Footnotes
    Commercial Relationships  J. Ruiz–Ederra, None; A.S. Verkman, None.
  • Footnotes
    Support  NIH, and Cystic Fibrosis Foundation: EY13574, DK35124, DK72517, EB00415, HL59198 and HL73856. JR–E was supported by a fellowship from Gobierno Vasco.
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 5422. doi:
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      J. Ruiz–Ederra, A.S. Verkman; Accelerated Cataract Formation in Aquaporin–1 Deficiency in Experiments Models of Cataractogenesis . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5422.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Two aquaporin (AQP)–type water channels are expressed in lens: AQP1 in surface epithelial cells, and AQP0 expressed in lens fiber cells. Mutations in AQP0 cause cataracts. The purpose of this study was to investigate the involvement of AQP1 in lens epithelial cell water permeability and maintenance of lens transparency in experimental models of cataract formation.

Methods: : AQP1 expression was detected by immunofluorescence in whole mounted lens and by immunoblot analysis. The role of AQP1 in lens epithelial water transport was determined by comparative measurements on lenses from wild–type and AQP1–null mice. Osmotic water permeability was measured in calcein–stained lens epithelial cells from the kinetics of fluorescence in response to externally applied osmotic gradients. Lens water content was measured by gravimetry using a kerosene/bromobenzene gradient (specific gravity 1.0950–1.1725). Lens transparency was measured by transmitted image contrast analysis in an in vitro model of high glucose–induced cataract formation (56 mM glucose).

Results: : AQP1 was expressed in epithelial cells of the anterior pole of the lens in wild–type mice and absent in AQP1–null mice. AQP1 deletion in mice did not alter baseline lens morphology or transparency. However, basal water content was significantly greater in AQP1 null mice, with specific gravities of 1.142 ±;0.001 (wild–type) and 1.132 ±;0.002 (AQP1–null). Plasma membrane water permeability in lens epithelium was reduced 2.8 ±;0.3–fold in AQP1 deficiency. Loss of transparency was approximately 3–fold accelerated in AQP1–null lenses bathed in a 55 mM glucose solution for 18 hours.

Conclusions: : Lens AQP1 facilitates the maintenance of transparency and opposes cataract formation, suggesting the possibility of AQP1 induction to retard cataractogenesis.

Keywords: cataract • pathology: experimental • crystalline lens 

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