December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Diabetes-Induced Retinal Vascular Permeability is Both Prevented and Reversed In Vivo by Oral Administration of PKC-ß Selective Inhibitor LY333531
Author Affiliations & Notes
  • AC Clermont
    Beetham Eye Institute Joslin Diabetes Center Boston MA
  • HI Salti
    Beetham Eye Institute Joslin Diabetes Center Boston MA
  • LE Goddard
    Beetham Eye Institute Joslin Diabetes Center Boston MA
  • GL King
    Beetham Eye Institute Joslin Diabetes Center Boston MA
  • LP Aiello
    Department of Ophthalmology Harvard Medical School Boston MA
  • Footnotes
    Commercial Relationships   A.C. Clermont, None; H.I. Salti, None; L.E. Goddard, None; G.L. King, Eli Lilly C, P; L.P. Aiello, Eli Lilly P, R. Grant Identification: EY10827 & RPB Dolly Green Scholarship
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3863. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      AC Clermont, HI Salti, LE Goddard, GL King, LP Aiello; Diabetes-Induced Retinal Vascular Permeability is Both Prevented and Reversed In Vivo by Oral Administration of PKC-ß Selective Inhibitor LY333531 . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3863.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: Since diabetes-induced retinal vascular permeability may be mediated by activation of protein kinase C (PKC), we examined whether primary and/or secondary intervention with orally-administered PKC-ß isoform-selective inhibitor LY333531 could prevent or reverse retinal vascular permeability in diabetic animals. Methods: STZ-induced diabetic (DM) and non-diabetic (NDM) Sprague-Dawley rats were assigned to a primary intervention (1°) group (treatment initiated at onset of DM with evaluation 2 weeks later) or a secondary (2°) intervention group (treatment begun 2w after onset of DM with evaluation 2w later). DM and NDM 1° groups were provided access to normal chow or chow containing 0.06% LY333531. The 2° groups received control chow for 2w followed by LY333531 or control chow for the subsequent 2w. Retinal vascular permeability was measured using the Evans-blue albumin permeation. Results: DM increased retinal vascular permeability as compared to NDM controls by 2.3±0.8 fold (n=8, p=0.042) and 2.5±0.7 fold (n=5, p=0.006) in the 1° and 2° groups, respectively. Preventative treatment with LY333531 reduced retinal vascular permeability by 92±50% (n=6, p=0.014) while interventional therapy resulted in a 100±32% (n=5, p=0.007) reduction as compared to untreated DM controls (1.3±0.8 vs 2.8±1.0 and 1.96±0.94 vs 4.85±1.35 µL/g/hr for 1o and 2o studies, respectively). LY333531 treatment of NDM groups did not alter retinal vascular permeability as compared to NDM controls (1.35±0.46 vs 1.21±1.25 and 2.27±0.67 vs 1.96±0.43 µL/g/hr for 1° and 2° studies, respectively). Conclusion: Two weeks of oral therapy with PKC-ß selective inhibitor LY33531 prevents diabetes-induced retinal vascular permeability and reverses the retinal vascular permeability already established after two weeks of diabetes. These data further suggest that the inhibition of PKC-ß in vivo may be a useful therapeutic approach for treatment of diabetic macular edema and similar disorders.

Keywords: 577 second messengers: pharmacology/physiology • 387 diabetes • 316 animal model 
×
×

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.

×