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Circular RNA Profiling in Peripheral Blood Mononuclear Cells from Retinopathy of Prematurity

ABSTRACT: Circular RNA Profiling in Peripheral Blood Mononuclear Cells from Retinopathy of Prematurity

PROVIDER: PRJNA842269 | ENA |

REPOSITORIES: ENA

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Circular RNA Profiling in Peripheral Blood Mononuclear Cells from Retinopathy of Prematurity

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Epithelial membrane protein-2 promotes VEGF signaling to promote pathological neovascular growth in retinopathy of prematurity

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Placental Inflammation Significantly Correlates with Reduced Risk for Retinopathy of Prematurity

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Placental Inflammation Significantly Correlates with Reduced Risk for Retinopathy of Prematurity

Project description:Retinopathy of prematurity (ROP), a blinding condition affecting preterm infants, accounts for up to 40% of all childhood blindness worldwide. ROP is an interruption of retinal vascular maturation, which is physiologically complete at full term and thus ongoing at the time of preterm birth. Although ROP demonstrates delayed onset following preterm birth, representing a window for therapeutic intervention, we cannot cure or prevent this disease. The in-utero environment, including placental function, is increasingly recognized for contributions to preterm infant disease risk. Herein, we examine the clinical associations between presence and severity of acute placental inflammation to ROP risk. Using logistic regression, we find a protective relationship between presence and severity of acute placental inflammation and preterm infant development of ROP. This is most significant for infants born in the absence of maternal preeclampsia. Further, we examine the underlying molecular mediators that may inform this protective paradigm. Adopting a candidate approach analyzing proteins with described ROP risk associations, we find that placental HTRA1 and FABP4 protein expression is significantly decreased within placental tissues characterized by acute inflammation. Additionally, HTRA1 and VEGFA demonstrate inverse longitudinal trends within the peripheral circulation for infants born in the presence compared to absence of acute placental inflammation. An agnostic approach, including whole transcriptome and differential methylation placental analysis, identifies novel mediators and pathways that may underly protection. Taken together, these data build on emerging literature showing disparate associations between acute placental inflammation and ROP development within preeclamptic or non-preeclamptic preterm infant populations and identifies novel placental mechanisms that may inform postnatal risk associations in preterm infants.

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