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Updated: Jan 3, 2026
Retinal Pathophysiological Evaluation in a Rat Model
Published on: May 6, 2022
Retinal proteomic evaluation of rats following streptozotocin‑injection using shotgun proteomics
Hiroko Otake1, Tetushi Yamamoto1, Saori Deguchi1
1Faculty of Pharmacy, Kindai University, Higashi-Osaka, Osaka 577‑8502, Japan.
Abstract:
It is important to elucidate how retinal stimulation leads to retinal protection and dysfunction. The current study aimed to identify factors that are up‑ and downregulated in the retinas of streptozotocin (STZ)‑induced diabetic rats with acute retinal dysfunction. Retinal function was measured and changes in protein expressions were determined using electroretinograms (ERGs) and liquid chromatography/mass spectroscopy‑based shotgun proteomics, respectively. The results revealed that the plasma glucose levels of STZ rats were markedly higher when compared with normal rats. Furthermore, levels of a‑waves, b‑waves and oscillatory potential amplitudes on ERGs in STZ rats were decreased compared with healthy animals. With use of shotgun proteomics, 391 proteins were identified in the retinas of normal rats and 541 proteins were found in the retinas of STZ rats. Of the 560 proteins identified in rat retinas, 372 (66.4%) were present in both normal and STZ rats. Of these, 19 (3.39%) were unique to normal rats and 169 (30.1%) were unique to STZ rats. Gene Ontology analysis was performed on the candidate proteins that were differentially regulated in the retinas of STZ rats and focused on those classified as 'protein binding', which serve important roles in retinal neurodegeneration. The results revealed an excessive expression of retinol‑binding protein 1 (RBP1) and a negative expression of rod outer segment membrane protein 1 (Rom-1) in the retinas of STZ rats. Therefore, retinal function may be decreased with STZ‑induced injury, and expressions of Rom‑1 and RBP1 may be altered in the retinas of STZ rats.
Insights
Diabetic retinopathy in rats involves decreased retinal function and altered protein levels. Specifically, streptozotocin-induced diabetic rats showed reduced electroretinogram waves and changes in retinol-binding protein 1 (RBP1) and rod outer segment membrane protein 1 (Rom-1) expression.
Area of Science:
- Ophthalmology
- Diabetic Retinopathy Research
- Proteomics
Background:
- Diabetic retinopathy is a significant complication of diabetes, leading to vision impairment.
- Understanding the molecular mechanisms underlying diabetic retinal dysfunction is crucial for developing effective treatments.
- Streptozotocin (STZ)-induced diabetes in rats serves as a model to study acute retinal changes.
Purpose of the Study:
- To identify proteins that are upregulated or downregulated in the retinas of STZ-induced diabetic rats.
- To correlate changes in protein expression with functional deficits in the retina.
- To investigate the role of specific proteins, such as RBP1 and Rom-1, in diabetic retinal injury.
Main Methods:
- Induction of diabetes in rats using streptozotocin (STZ).
- Assessment of retinal function using electroretinograms (ERGs) to measure a-waves, b-waves, and oscillatory potentials.
- Quantitative proteomic analysis using liquid chromatography/mass spectrometry (LC-MS)-based shotgun proteomics to identify and quantify retinal proteins.
Main Results:
- STZ-induced diabetic rats exhibited significantly higher plasma glucose levels and decreased ERG amplitudes compared to normal rats.
- Shotgun proteomics identified differential protein expression in the retinas of STZ rats, with 169 proteins unique to this group.
- Gene Ontology analysis highlighted altered expression of 'protein binding' factors, notably increased retinol-binding protein 1 (RBP1) and decreased rod outer segment membrane protein 1 (Rom-1).
Conclusions:
- STZ-induced diabetes causes acute retinal dysfunction in rats, evidenced by impaired ERG responses.
- Proteomic analysis reveals significant alterations in retinal protein expression profiles in diabetic conditions.
- The dysregulation of RBP1 and Rom-1 may play a role in the pathogenesis of STZ-induced diabetic retinopathy.
