April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Aquaporin-0 Targets Interlocking Protrusions to Control Integrity and Transparency of the Mouse Lens
Author Affiliations & Notes
  • Woo-Kuen Lo
    Neurobiology, Morehouse School of Medicine, Atlanta, GA
  • Sondip K Biswas
    Neurobiology, Morehouse School of Medicine, Atlanta, GA
  • Lawrence Brako
    Neurobiology, Morehouse School of Medicine, Atlanta, GA
  • Alan Shiels
    Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO
  • Sumin Gu
    Biochemistry, University of Texas Health Science Center, San Antonio, TX
  • Jean X Jiang
    Biochemistry, University of Texas Health Science Center, San Antonio, TX
  • Footnotes
    Commercial Relationships Woo-Kuen Lo, None; Sondip Biswas, None; Lawrence Brako, None; Alan Shiels, None; Sumin Gu, None; Jean Jiang, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1684. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Woo-Kuen Lo, Sondip K Biswas, Lawrence Brako, Alan Shiels, Sumin Gu, Jean X Jiang; Aquaporin-0 Targets Interlocking Protrusions to Control Integrity and Transparency of the Mouse Lens. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1684.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Lens fiber cell membranes contain aquaporin-0 (AQP0) which constitutes approximately 50% of total integral fiber-cell membrane proteins and plays a dual function as a water channel protein and an adhesion molecule. Fiber cell membranes also develop an elaborate interlocking system that is required for maintaining the structural order, stability and lens transparency. Here we use an AQP0-deficient mouse model to investigate an unconventional adhesion role of AQP0 in maintaining a normal structure of interlocking protrusions in the lens.

Methods: The loss of AQP0 in lens fibers of AQP0-/- mice was verified by a purified AQP0 polyclonal antibody using Western blotting and immunofluorescence analyses. Changes in membrane surface structures of lens fibers of wild-type and AQP0-/- mice at 3 to 12 weeks old were examined with scanning electron microscopy. Preferential distribution of AQP0 in fiber cell membranes in wild-type controls was analyzed with confocal immunofluorescence and immunogold labeling using freeze-fracture TEM.

Results: Interlocking protrusions in young differentiating fiber cells developed normally but showed minor abnormalities at approximately 50 μm deep from the surface in the absence of AQP0 in all ages studied. Strikingly, interlocking protrusions in maturing fiber cells specifically underwent uncontrolled elongation, deformation and fragmentation while the cells still possessed fairly normal configurations in the early process. These changes eventually resulted in fiber-cell separation, breakdown and cataract formation in the lens core. Immunolabeling at the light and electron microscopic levels demonstrated that AQP0 was particularly enriched in interlocking protrusions in wild-type lenses.

Conclusions: This study suggests that AQP0 exerts its primary adhesion or suppression role specifically to maintain the normal structure of interlocking protrusions that is critical to the integrity and transparency of the lens.

Keywords: 446 cell adhesions/cell junctions • 448 cell membrane/membrane specializations • 597 microscopy: electron microscopy  
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×