Publications by authors named "Anne Gro W Rognlien"
Article Synopsis
- The study investigates how exposure to high oxygen levels affects retinal gene expression in mice with a model of oxygen-induced retinopathy (OIR), which resembles retinopathy of prematurity.
- Mice were subjected to 75% oxygen for 5 days, and their retinal samples were analyzed for gene expression to identify changes during neovascularization and regression phases.
- Key findings highlight the enrichment of specific signaling pathways, including those related to apoptosis and immune responses, suggesting these pathways play a significant role in the disease's development and progression.
Article Synopsis
- This study investigates gene expression patterns in blood and retina of mice with oxygen-induced retinopathy (OIR), a model for retinopathy of prematurity, to better understand the disease and identify potential blood biomarkers.
- 120 C57BL/6J mice were used, divided into an OIR group exposed to high oxygen levels and a control group, with gene expression analyzed from blood and retinal cells over a period of 28 days using microarrays.
- Results revealed significant changes in gene expression, especially in the retina, with specific genes (Deptor and Nol4) showing decreased expression in both blood and retina on day 17, suggesting they could be linked to retinal neovascularization and warrant further exploration.
Background: Bronchopulmonary dysplasia (BPD) is a common cause of abrupted lung development after preterm birth. BPD may lead to increased rehospitalization, more severe and frequent respiratory infections, and life-long reduced lung function. The gene regulation in lungs with BPD is complex, with various genetic and epigenetic factors involved.
View Article and Find Full Text PDFTo examine the gene expression regarding pulmonary vascular disease in experimental bronchopulmonary dysplasia in young mice. Premature delivery puts babies at risk of severe complications. Bronchopulmonary dysplasia (BPD) is a common complication of premature birth leading to lifelong affection of pulmonary function.
View Article and Find Full Text PDFBackground 8-Oxoguanine DNA-glycosylase 1 (OGG1) and mutY DNA glycosylase (MUTYH) are crucial in the repair of the oxidative DNA lesion 7,8-dihydro-8-oxoguanine caused by hypoxia-reoxygenation injury. Our objective was to compare the gene expression changes after hypoxia-reoxygenation in neonatal Ogg1-Mutyh double knockout mice (OM) and wildtype mice (WT), and study the gene response in OM after hyperoxic reoxygenation compared to normoxic. Methods Postnatal day 7 mice were subjected to 2 h of hypoxia (8% O2) followed by reoxygenation in either 60% O2 or air, and sacrificed right after completed reoxygenation (T0h) or after 72 h (T72h).
View Article and Find Full Text PDFBackground: One out of four children with neonatal asphyxia has lung involvement. Still, there has been little research on injury mechanisms of hypoxia-reoxygenation in the neonatal lung.
Objectives: To make a temporal profile of the gene expression changes of 44 a priori selected genes after hypoxia-reoxygenation in the newborn mouse lung, and to compare the changes after hyperoxic and normoxic reoxygenation.
Background: Hyperoxic reoxygenation following hypoxia increases the expression of inflammatory genes in the neonatal mouse brain. We have therefore compared the temporal profile of 44 a priori selected genes after hypoxia and hyperoxic or normoxic reoxygenation.
Methods: Postnatal day 7 mice were subjected to 2 h of hypoxia (8% O2) and 30 min reoxygenation with 60% or 21% O2.