June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Ranibizumab treatment protects retinal cells in an ischemia model
Author Affiliations & Notes
  • Stephanie C Joachim
    Experimental Eye Research Institute, Ruhr University, Bochum, Germany
  • Marina Renner
    Experimental Eye Research Institute, Ruhr University, Bochum, Germany
  • Sabrina Reinehr
    Experimental Eye Research Institute, Ruhr University, Bochum, Germany
  • Gesa Stute
    Experimental Eye Research Institute, Ruhr University, Bochum, Germany
  • Carsten Theiss
    Department of Cytology, Institute of Anatomy, 'Bochum, Germany
  • Burkhard Dick
    Experimental Eye Research Institute, Ruhr University, Bochum, Germany
  • Footnotes
    Commercial Relationships Stephanie Joachim, None; Marina Renner, None; Sabrina Reinehr, None; Gesa Stute, None; Carsten Theiss, None; Burkhard Dick, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2478. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to Subscribers Only
      Sign In or Create an Account ×
    • Get Citation

      Stephanie C Joachim, Marina Renner, Sabrina Reinehr, Gesa Stute, Carsten Theiss, Burkhard Dick; Ranibizumab treatment protects retinal cells in an ischemia model. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2478.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Retinal ischemia is common in eye disorders, like diabetic retinopathy or retinal vascular occlusion. The goal of this study was to evaluate the effects of an intravitreally injected vascular endothelial growth factor (VEGF) inhibitor (Ranibizumab) on retinal cells in an ischemia-reperfusion animal model (I/R).

Methods: I/R was induced in adult Brown Norway rats and one half was treated with Ranibizumab (10 mg/ml) three days later. The control group did not undergo I/R or treatment (n=6-8/group). After 3 weeks aqueous humor VEGF levels were measured via ELISA. Retinal cross-sections were stained with H&E, Brn-3a (retinal ganglion cells), rhodopsin (photoreceptors), ChAT (amacrine cells), GFAP (macroglia), and VEGF-R2 (VEGF-receptor). Cell counts and staining area evaluation was performed using ImageJ followed by statistical analysis (Statistica).

Results: A significant VEGF increase was detected in aqueous humor of I/R eyes (p=0.02), but not in Ranibizumab ones (p=0.9). I/R retinas showed significantly lower RGC numbers (16.7±3.0 cells/mm; p=0.001) compared to controls (34.5±1.7 cells/mm). Numbers in the Ranibizumab group (31.4±3.3 cells/mm) were comparable to controls (p=0.2). The rhodopsin+ area was significantly reduced in the I/R group (I/R: 9.1±1.2%; control: 12.9±0.9%; p=0.02). The Ranibizumab group (15.2±1.1%) had a significantly greater rhodopsin+ area than the I/R group (p<0.001). In the I/R and Ranibizumab group a decreased ChAT score was observed (p<0.001). Also, fewer ChAT+ cells were noted in these groups (p<0.001). VEGF-R2 was highly expressed in I/R retinas (p=0.006), but not in Ranibizumab ones (p=0.4). Also, a stronger GFAP response was observed in I/R (p=0.01) than in Ranibizumab retinas (p=0.4).

Conclusions: Ranibizumab treatment protects retinal cells, like RGCs and photoreceptors against ischemic damage. Only amacrine cells could not be rescued. These cells seem to be particularly sensitive to this damage. Possibly, an earlier intervention is necessary to protect amacrine cells in this 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.

×