Biomolecular Effects of Jb1 (an IGF-I Peptide Analog) in a Rat Model of Oxygen-Induced Retinopathy

被引:14
作者
Brock, Romy S.
Gebrekristos, Bisrat H. [2 ]
Kuniyoshi, Katherine M. [2 ]
Modanlou, Houchang D.
Falcao, Mario Cicero [3 ]
Beharry, Kay D. [1 ]
机构
[1] Univ Calif Irvine, Div Neonatol, Dept Pediat, Orange, CA 92868 USA
[2] Miller Childrens Hosp, Dept Pediat, Long Beach, CA 90806 USA
[3] Univ Sao Paolo, Dept Pediat, BR-03071000 Sao Paulo, Brazil
关键词
GROWTH-FACTOR-I; RETINAL NEOVASCULARIZATION; NEONATAL-RAT; VEGF; INHIBITION; BIRTH; PREMATURITY; RECEPTOR; HYPOXIA; HYPEROXIA;
D O I
10.1203/PDR.0b013e318204e6fa
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
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 mu g/d) on P1, P2, and P3 (JB1x3); 2) JB1 (1 mu g/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 O-2. 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. (Pediatr Res 69: 135-141, 2011)
引用
收藏
页码:135 / 141
页数:7
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