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J. Biol. Chem., Vol. 277, Issue 21, 19139-19144, May 24, 2002
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From the Departments of Medicine and Physiology, Cardiovascular
Research Institute, University of California, San Francisco,
California 94143-0521
Two aquaporin (AQP)-type water channels are
expressed in mammalian cornea, AQP1 in endothelial cells and AQP5 in
epithelial cells. To test whether these aquaporins are involved in
corneal fluid transport and transparency, we compared corneal
thickness, water permeability, and response to experimental swelling in
wild type mice and transgenic null mice lacking AQP1 and AQP5. Corneal thickness in fixed sections was remarkably reduced in AQP1 null mice
and increased in AQP5 null mice. By z-scanning confocal microscopy, corneal thickness in vivo was (in µm, mean ± S.E.,
n = 5 mice) 123 ± 1 (wild type), 101 ± 2 (AQP1 null), and 144 ± 2 (AQP5 null). After exposure of the
external corneal surface to hypotonic saline (100 mosM), the rate of corneal swelling (5.0 ± 0.3 µm/min, wild type) was reduced by AQP5 deletion (2.7 ± 0.1 µm/min). After exposure of the endothelial surface to hypotonic
saline by anterior chamber perfusion, the rate of corneal swelling
(7.1 ± 1.0 µm/min, wild type) was reduced by AQP1 deletion
(1.6 ± 0.4 µm/min). Base-line corneal transparency was not
impaired by AQP1 or AQP5 deletion. However, the recovery of corneal
transparency and thickness after hypotonic swelling (10-min exposure of
corneal surface to hypotonic saline) was remarkably delayed in AQP1
null mice with ~75% recovery at 7 min in wild type mice compared
with 5% recovery in AQP1 null mice. Our data indicate that AQP1 and
AQP5 provide the principal routes for corneal water transport across
the endothelial and epithelial barriers, respectively. The impaired
recovery of corneal transparency in AQP1 null mice provides evidence
for the involvement of AQP1 in active extrusion of fluid from the
corneal stroma across the corneal endothelium. The up-regulation of
AQP1 expression and/or function in corneal endothelium may reduce
corneal swelling and opacification following injury.
Aquaporin Deletion in Mice Reduces Corneal Water Permeability and
Delays Restoration of Transparency after Swelling*
*
This work was supported by Grants EY13574, EB00415, DK35124,
HL59198, HL60288, and DK43840 from the National Institutes of Health
and a grant from the Cystic Fibrosis Foundation.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Cardiovascular
Research Institute, 1246 Health Sciences East Tower, Box 0521, University of California, San Francisco, San Francisco, CA 94143-0521. Tel.: 415-476-8530; Fax: 415-665-3847; E-mail: verkman@itsa.ucsf.edu; Website: www.ucsf.edu/verklab.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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