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Updated: Jan 21, 2026
09:28
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
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Retinal proteome associated with bradykinin-induced edema
Nivetha Murugesan1, Ward Fickweiler2, Allen C Clermont2
1Joslin Diabetes Center, Boston, MA, USA; KalVista Pharmaceuticals Inc, Cambridge, MA, USA.
Experimental Eye Research
|July 28, 2019
Summary
Bradykinin (BK) causes retinal thickening and alters protein levels in rat retinas, similar to changes seen in diabetic macular edema (DME). This study identifies specific proteins, including complement C3, affected by BK, offering insights into DME pathogenesis.
Area of Science:
- Ophthalmology
- Proteomics
- Molecular Biology
Background:
- Diabetic macular edema (DME) is linked to bradykinin (BK) generation.
- Understanding BK's effects on retinal structure and protein expression is crucial for DME research.
Purpose of the Study:
- To characterize the ultrastructural and proteomic changes in the rat retina induced by intravitreal bradykinin (BK) injection.
- To compare BK-induced retinal changes with those induced by vascular endothelial growth factor (VEGF).
- To identify proteins altered by BK that are also found in human DME vitreous.
Main Methods:
- Intravitreal injections of BK or VEGF in Sprague Dawley rats.
- Spectral-domain optical coherence tomography (OCT) to assess retinal thickness and vascular ultrastructure.
- Mass spectrometry-based proteomics to analyze retinal protein expression.
- Western blot analysis to validate protein level changes.
Main Results:
- BK and VEGF injections caused transient increases in retinal thickness and vascular tortuosity.
- Proteomic analysis identified 1757 non-redundant proteins; 18 proteins decreased and 32 increased significantly in BK-injected retinas.
- Eight proteins, including complement C3, were elevated in BK-treated rat retinas and human DME vitreous samples.
- Complement 3 levels were significantly increased in both BK-injected rat vitreous and clinical DME samples.
Conclusions:
- BK induces significant changes in retinal ultrastructure and proteome in rats.
- Several BK-affected proteins, notably complement C3, are implicated in DME pathogenesis.
- This study provides a molecular basis for BK's role in DME and identifies potential therapeutic targets.
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