March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
COMPAng1 Prevents Decreases in Visual Acuity and Retinal Thinning in the Diabetic Mouse
Author Affiliations & Notes
  • Judd M. Cahoon
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Hironori Uehara
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Ling Luo
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Thomas K. Olsen
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Tadashi R. Miya
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Vainu'Upo R. Jessop
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Bonnie J. Archer
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Bala K. Ambati
    Ophthalmology & Visual Sciences, University of Utah, Salt Lake City, Utah
  • Footnotes
    Commercial Relationships  Judd M. Cahoon, None; Hironori Uehara, None; Ling Luo, None; Thomas K. Olsen, None; Tadashi R. Miya, None; Vainu'Upo R. Jessop, None; Bonnie J. Archer, None; Bala K. Ambati, None
  • Footnotes
    Support  NEI R01 EY017182-01A2
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5758. doi:
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      Judd M. Cahoon, Hironori Uehara, Ling Luo, Thomas K. Olsen, Tadashi R. Miya, Vainu'Upo R. Jessop, Bonnie J. Archer, Bala K. Ambati; COMPAng1 Prevents Decreases in Visual Acuity and Retinal Thinning in the Diabetic Mouse. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5758.

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

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Abstract
 
Purpose:
 

Vascular dysfunction plays a role in many pathologies. Normalizing the vasculature is a potential mechanism to combat deficiencies induced by a failing vascular tree. Diabetic macular edema resulting from vascular hyperpermeability is the leading cause of vision loss in working-age Americans. Angiopoietin-1 plays a critical role in the development of macular edema due to its effects on vascular permeability. Here, we treat diabetic mice with a stable soluble variant of angiopoietin 1, COMP-Ang1, to mitigate vascular leakage and the hallmarks of ischemia associated with diabetes.

 
Methods:
 

Diabetic mice (type 1 diabetic Akita Ins2+/-, type 2 diabetic db/db) were treated at 2 months of age with one intravitreal injection of an adeno associated virus expressing COMPAng1, AcGFP, or phosphate buffered saline as control. Hallmarks of ischemic retinopathy were assessed over the next four months including retinal thickness (as measured by optical coherence tomography) visual acuity (as measured by OptoMotry), as well as vessel area (as observed using immunohistochemistry), vascular hyperpermeability (as assessed by Evans blue dye), and protein expression (as assessed by Western blot).

 
Results:
 

COMPAng1 prevented diabetes-induced decreases in retinal ganglion cell layer thickness (14.9 +/- 3.1 um treated vs. 8.1 +/- 1.7 um control, p < 0.05) and visual acuity (0.307 +/- 0.08 cycles/degree treated vs. 0.11 +/- 0.11 control, p < 0.05). Vascular area was returned to non-diabetic control levels (21% vs. 16% vessel area (isolectin positive)/total area p 0.05). Furthermore, COMP-Ang1 treatment increased VE-cadherin stability and decreased VEGF-A expression. Vascular hyperpermeability was reduced in COMPAng1 treated diabetic mice compared to control (.0020 +/- 0.0008 vs. 0.0072 +/- 0.0004 absorbance, p < 0.05).

 
Conclusions:
 

We propose that COMP-Ang1 not only directly prevents vascular leak by stabilizing VE-cadherin but the normalized vasculature also adequately perfuses tissue resulting in less hypoxia-driven VEGF secretion. COMP-Ang1 promotes vascular integrity, prevents retinal ischemia, and decreases vascular permeability through suppression of VEGF-A expression and could be useful in the treatment of non-proliferative diabetic retinopathy.  

 
Keywords: diabetic retinopathy • electroretinography: non-clinical • hypoxia 
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