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Updated: Jun 6, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Biomolecular effects of JB1 (an IGF-I peptide analog) in a rat model of oxygen-induced retinopathy
Romy S Brock1, Bisrat H Gebrekristos, Katherine M Kuniyoshi
1Department of Pediatrics, University of California Irvine, Irvine, California 92868, USA.
Insights
Early, short-term treatment with an IGF-I analog (JB1) effectively prevented retinopathy in a rat model. This intervention normalized retinal abnormalities by potentially involving soluble VEGFR-1.
Area of Science:
- Ophthalmology
- Neonatology
- Endocrinology
Background:
- Low serum Insulin-like Growth Factor-I (IGF-I) is a risk factor for retinopathy of prematurity in extremely low birth weight infants.
- Oxygen-induced retinopathy is a significant concern in premature infants.
Purpose of the Study:
- To investigate the potential of JB1, an IGF-I analog, in preventing oxygen-induced retinopathy in a neonatal rat model.
- To evaluate the efficacy of different JB1 treatment durations on retinal pathology.
Main Methods:
- Neonatal rats were exposed to cyclic hyperoxia/hypoxia (H/H) from birth to P14.
- Treatment groups received subcutaneous injections of JB1 (short-term: JB1x3; prolonged: JB1x7) or saline.
- Systemic and ocular factors including VEGF, soluble VEGFR-1 (sVEGFR-1), IGF-I, and retinal vasculature were assessed.
Main Results:
- Short-term JB1 treatment (JB1x3) was more effective than prolonged treatment (JB1x7) in reducing retinal pathologies.
- JB1x3 treatment was associated with increased levels of sVEGFR-1.
- Retinal abnormalities induced by H/H cycling were normalized by early, short-term JB1 exposure.
Conclusions:
- Early, short-term systemic JB1 treatment can normalize retinal abnormalities in a model of oxygen-induced retinopathy.
- The protective effect of JB1 may be mediated through modulation of sVEGFR-1 levels.
- This study highlights a potential therapeutic strategy for retinopathy of prematurity.
Abstract:
Low-serum IGF-I levels at birth is a risk factor for the development of retinopathy of prematurity in extremely LBW infants. We tested the hypothesis that JB1 (an IGF-I analog) prevents oxygen-induced retinopathy in our rat model. Neonatal rats were exposed to 50% oxygen with brief, clustered, hypoxic (12%) episodes from birth to P14. The pups were treated with s.c. injections of 1) JB1 (1 μg/d) on P1, P2, and P3 (JB1x3); 2) JB1 (1 μg/d) on alternate days from P1 to P13 (JB1x7); or 3) equivalent volume saline. Control littermates were raised in room air (RA) with all conditions identical except for inspired O2. Groups were analyzed after hyperoxia/hypoxia (H/H) cycling at P14 or allowed to recover in RA until P21. Systemic and ocular VEGF, soluble VEGFR-1, and IGF-I; retinal vasculature; and gene profile of retinal angiogenesis were assessed. JB1x3 was more effective with associated increases in sVEGFR-1 and decreased retinal pathologies than JB1x7. We conclude that early short-term exposure to systemic JB1 treatment normalizes retinal abnormalities seen with H/H cycling, an effect that may involve sVEGFR-1.
