Postnatal Serum Insulin-Like Growth Factor I and Retinopathy of Prematurity

Jensen, Anne K.; Ying, Gui‐Shuang; Huang, Jiayan; Quinn, Graham E.; Binenbaum, Gil

doi:10.1097/iae.0000000000001247

Cited by 49 publications

(30 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is well known that preterm infants who are at the highest risk for development of severe ROP are more likely to be growth suppressed. Poor growth and low systemic IGF-I levels have been shown to be important predictors of severe ROP [36,37]. The computerized clinical algorithm Weight, Insulin-like growth factor (IGF-1), Neonatal Retinopathy of Prematurity (WINROP) has been developed as a non-invasive tool for identifying infants at risk for ROP based on postnatal weight gain and IGF-I levels [56].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Bumetanide Suppression of Angiogenesis in a Rat Model of Oxygen-Induced Retinopathy

Guzel

Cai

Ahmad

et al. 2020

IJMS

View full text Add to dashboard Cite

Aquaporins (AQPs) are involved in hypoxia-induced angiogenesis and retinal damage. Bumetanide is a diuretic agent, Na+/K+/Cl− cotransporter (NKCC1), and AQP 1–4 inhibitor. We tested the hypothesis that early postnatal treatment with bumetanide suppresses biomarkers of angiogenesis and decreases severe retinopathy oxygen-induced retinopathy (OIR). Neonatal rats were exposed at birth (P0) to either (1) room air (RA); (2) hyperoxia (50% O2); or (3) intermittent hypoxia (IH) consisting of 50% O2 with brief, clustered episodes of 12% O2 from P0 to postnatal day 14 (P14), during which they were treated intraperitoneally (IP) with bumetanide (0.1 mg/kg/day) or an equivalent volume of saline, on P0–P2. Pups were examined at P14 or allowed to recover in RA from P14–P21. Retinal angiogenesis, morphometry, pathology, AQPs, and angiogenesis biomarkers were determined at P14 and P21. Bumetanide reduced vascular abnormalities associated with severe OIR. This was associated with reductions in AQP-4 and VEGF. Bumetanide suppressed sVEGFR-1 in the serum and vitreous fluid, but levels were increased in the ocular tissues during recovery. Similar responses were noted for IGF-I. In this model, early systemic bumetanide administration reduces severe OIR, the benefits of which appear to be mediated via suppression of AQP-4 and VEGF. Further studies are needed to determine whether bumetanide at the right doses may be considered a potential pharmacologic agent to treat retinal neovascularization.

show abstract

Section: Discussionmentioning

confidence: 99%

“…IGF-I is a permissive factor for VEGF, and serum levels have been shown to be deficient in preterm infants who developed severe ROP [6,36,37]. Serum and vitreous fluid IGF-I levels at P14 and P21 are presented in Figure 7.…”

Section: Effect Of Bumetanide On Igf-1 Levelsmentioning

confidence: 99%

Bumetanide Suppression of Angiogenesis in a Rat Model of Oxygen-Induced Retinopathy

Guzel

Cai

Ahmad

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…Studies have shown that low serum IGF‐1 is associated with development of severe ROP 48, 49, 50. IGF‐1 supplementation may be a treatment option to prevent the occlusion of vasculature during the first phase of ROP.…”

Section: Discussionmentioning

confidence: 99%

Up‐regulated basigin‐2 in microglia induced by hypoxia promotes retinal angiogenesis

Yin

et al. 2017

J Cellular Molecular Medi

View full text Add to dashboard Cite

Retinal microglia cells contribute to vascular angiogenesis and vasculopathy induced by relative hypoxia. However, its concrete molecular mechanisms in shaping retinal angiogenesis have not been elucidated. Basigin, being involved in tumour neovasculogenesis, is explored to exert positive effects on retinal angiogenesis induced by microglia. Therefore, we set out to investigate the expression of basigin using a well‐characterized mouse model of oxygen‐induced retinopathy, which recapitulated hypoxia‐induced aberrant neovessel growth. Our results elucidate that basigin is overexpressed in microglia, which accumulating in retinal angiogenic sprouts. In vitro, conditioned media from microglia BV2 under hypoxia treatment increase migration and tube formation of retinal capillary endothelia cells, compared with media from normoxic condition. The angiogenic capacity of BV2 is inhibited after basigin knockdown by small interfering RNAs. A new molecular mechanism for high angiogenic capacity, whereby microglia cells release basigin via up‐regulation of PI3K‐AKT and IGF‐1 pathway to induce angiogenesis is unveiled. Collectively, our results demonstrate that basigin from hypoxic microglia plays a pivotal pro‐angiogenic role, providing new insights into microglia‐promoting retinal angiogenesis.

show abstract

“…Extremely preterm infants are at high risk of developing morbidities, including retinopathy of prematurity (ROP), a multifactorial disease with a complex pathogenesis that is not yet fully understood. We and others have identified low postnatal levels of IGF-I as a strong risk factor for ROP [1–3]. Other factors beyond low gestational age (GA) at birth and low postnatal levels of IGF-I that have been identified as risk factors for ROP include low birth weight and poor postnatal growth, sub-optimal oxygen therapy, depletion of the maternal supply of growth and nutritional factors, and red blood cell transfusion [1,4–6].…”

Section: Introductionmentioning

confidence: 99%

Increased postnatal concentrations of pro-inflammatory cytokines are associated with reduced IGF-I levels and retinopathy of prematurity

Hellgren

Löfqvist

Hansen‐Pupp

et al. 2018

Growth Hormone & IGF Research

View full text Add to dashboard Cite

Objective Retinopathy of prematurity (ROP) is a multifactorial disease linked to low insulin-like growth factor (IGF)-I levels and perhaps to postnatal inflammation. Here, we investigated the longitudinal postnatal serum concentrations of pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α in relation to IGF-I levels and ROP. Design The study cohort included 52 infants born before 31 gestational weeks. The infants were screened for ROP and classified as non-ROP (n = 33), non-proliferative ROP (stages 1 and 2; n = 10), or proliferative ROP (stage 3, all treated for ROP; n = 9). Blood samples were collected at birth, 24 h after birth, and then weekly until at least 36 weeks postmenstrual age (PMA) (i.e., up to 13 weeks after birth). Circulating levels of IL-6 and TNF-α were evaluated in relation to circulating IGF-I levels and ROP. Results IL-6 levels negatively correlated with IGF-I levels between 5 and 8 weeks after birth, (p < 0.01 to p < 0.05). At birth, the IL-6 and TNF-α levels were similar independent of later ROP. Twenty-four hours after birth, both IL-6 and TNF-α levels had increased in infants later treated for ROP (p < 0.05). Postnatal, infants treated for ROP had higher IL-6 levels than infants without ROP. Conclusions The pro-inflammatory response is associated with low IGF-I levels and the development of ROP.

show abstract

Postnatal Serum Insulin-Like Growth Factor I and Retinopathy of Prematurity

Cited by 49 publications

References 35 publications

Bumetanide Suppression of Angiogenesis in a Rat Model of Oxygen-Induced Retinopathy

Bumetanide Suppression of Angiogenesis in a Rat Model of Oxygen-Induced Retinopathy

Up‐regulated basigin‐2 in microglia induced by hypoxia promotes retinal angiogenesis

Increased postnatal concentrations of pro-inflammatory cytokines are associated with reduced IGF-I levels and retinopathy of prematurity

Contact Info

Product

Resources

About