Project description:To reveal the altered expression profiles of circular RNAs (circRNAs) in the peripheral blood mononuclear cells (PBMCs) of patients with retinopathy of prematurity (ROP), microarray analysis was conducted in the samples from ROP patients and controls.

2022-08-10 | GSE204780 | GEO

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

Project description:Retinopathy of prematurity (ROP) is a leading cause of childhood blindness, and exclusively affects infants born prematurely. In this study, we test the hypothesis that EMP2 contributes to neovascularization in a mouse model of the disease. We show that EMP2 promotes neuronal VEGF signaling and that its downregulation reduces severity of neovascularization.

2021-12-17 | GSE123945 | GEO

GENEVA GWAS of Prematurity and its Complications - African Ancestry

Project description:GENEVA GWAS of Prematurity and its Complications - African Ancestry

| PRJNA75465 | ENA

GENEVA GWAS of Prematurity and its Complications - European Ancestry

Project description:GENEVA GWAS of Prematurity and its Complications - European Ancestry

| PRJNA75461 | ENA

Project description:Clinical and genetic analysis of retinopathy of prematurity

| PRJNA623135 | ENA

Gene expression microarray analysis of early oxygen-induced retinopathy (OIR)

Project description:Different inbred strains of rats differ in their susceptibility to OIR, an animal model of human retinopathy of prematurity. We examined gene expression profiles in Fischer 344 (F344, resistant to OIR) and Sprague Dawley (SD, susceptible to OIR) rats at the early time point of day 3 to identifying gene pathways related to the underlying genetic cause of phenotypic differences between strains.

2009-11-13 | GSE18998 | GEO

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.

2023-01-01 | GSE218039 | GEO

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