Transcriptome analysis in very preterm infants with chronic lung disease after birth
|Study ID||Alternative Stable ID||Type|
Bronchopulmonary dysplasia (BPD) is the most common complication of prematurity and is characterized by impaired alveolar and vascular development. The aim of the study was to identify early BPD-relevant pathways by applying whole genome transcriptional profiling combined with protein measurements from umbilical arterial blood samples of preterm infants with and without BPD. Only newborn infants <32 weeks gestational age (GA) were prospectively included in this study. Blood was obtained from an indwelling umbilical artery catheter at birth and after 72 hours after birth and subjected to gene expression analysis using the Codelink Human I 10k Bioarray and the the Codelink Human Whole Genome Bioarray. The study reveals a monocyte-centered immune response at birth characterizing preterm infants later developing BPD. The findings provide potential markers for early risk stratification in the preterm infant with respect to the development of chronic pulmonary disease and may subsequently enable the development of new treatment strategies in this high risk patient cohort.
Study Datasets 2 dataset.
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|EGAD00010001424||Codelink Human Whole Genome from Blood taken at 72 hours after birth (11 cases)||Codelink Human Whole Genome Bioarray||11|
|EGAD00010001425||Codelink Human Whole Genome from Blood taken at 72 hours after birth (9 controls)||Codelink Human Whole Genome Bioarray||9|
Who archives the data?
Attenuated PDGF signaling drives alveolar and microvascular defects in neonatal chronic lung disease.
EMBO Mol Med 9:2017 1504-1520