May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
The Role of Protein Kinase C (pkc) in the Regulation of Fluid Transport Across Rabbit Corneal Endothelium
Author Affiliations & Notes
  • F. P. Diecke
    Pharmacology and Physiology, UMD New Jersey Medical School, Newark, New Jersey
  • L. Ma
    Columbia University, New York, New York
  • P. Iserovich
    Ophthalmology, Columbia, New York, New York
  • J. Fischbarg
    Columbia University, New York, New York
  • Footnotes
    Commercial Relationships F.P. Diecke, None; L. Ma, None; P. Iserovich, None; J. Fischbarg, None.
  • Footnotes
    Support EY06178; RPB
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 3998. doi:
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    • Get Citation

      F. P. Diecke, L. Ma, P. Iserovich, J. Fischbarg; The Role of Protein Kinase C (pkc) in the Regulation of Fluid Transport Across Rabbit Corneal Endothelium. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3998.

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

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Purpose:: The regulation of fluid transport across the corneal endothelium by extra- and intracellular messengers is poorly understood. We have examined the effects of modulation of PKC with activators and inhibitors on corneal fluid transport.

Methods:: Corneas were obtained from New Zealand albino rabbits (~2 kg) using procedures in accordance with NIH guidelines. Transendothelial fluid movement was determined by measuring the changes in corneal thickness with the Dikstein-Maurice method. Corneal thickness was determined with a computer-controlled specular microscope, which automatically sensed and recorded it at 5-minute intervals. Fluid transport was calculated from the rates of corneal thickness change as reported previously.

Results:: Inhibition of PKC activity with calphostin C, an inhibitor of conventional and novel PKC isoforms, resulted in a dose-dependent increase in fluid movement and a reduction of corneal thickness. The effect of PKC activators was found to be more complex. Phorbol-12, 13- dibutyrate (PDBu) and Phorbol-12-myristate-13-acetate (PMA) produce an initial increase followed by a reduction in fluid transport. We have further attempted to identify the membrane component affected by PKC modulation. Corneal swelling in bicarbonate-free solutions was temporarily arrested by exposure to 1 µM calphostin C. However, if corneal swelling was induced by inhibition of anion channels using a cocktail of 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumic acid (NA) both 100 µM, then exposure to Calphostin C did not affect the rate of swelling.

Conclusions:: Activation of PKC may result in an initial activation of fluid transport followed by inhibition of it. Such activation and/or inhibition may be due to effects on anion channels.

Keywords: cornea: endothelium • ion transporters • ion channels 

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