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  • Title: Biomolecular effects of JB1 (an IGF-I peptide analog) in a rat model of oxygen-induced retinopathy.
    Author: Brock RS, Gebrekristos BH, Kuniyoshi KM, Modanlou HD, Falcao MC, Beharry KD.
    Journal: Pediatr Res; 2011 Feb; 69(2):135-41. PubMed ID: 21057375.
    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.
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