Project description:We performed miRNA and mRNA profiling at postnatal day 14 and day 29 to compare hyperoxia-induced bronchopulmonary dysplasia and wild type. We built potential miRNA-mRNA interaction networks specific to brochopulmonary dysplasia. Replicated time course of mouse lung development at 2 time points (P14, P29). Three replicates per time point for bronchopulmonary dysplasia induced by hyperoxia mouse lung, and two replicates per time point for wild type mouse lung. This dataset represents the mRNA expression profiling component of the study.
Project description:We performed miRNA and mRNA profiling at postnatal day 14 and day 29 to compare hyperoxia-induced bronchopulmonary dysplasia and wild type. We built potential miRNA-mRNA interaction networks specific to brochopulmonary dysplasia. Replicated time course of mouse lung development at 2 time points (P14, P29). Three replicates per time point for bronchopulmonary dysplasia induced by hyperoxia mouse lung, and two replicates per time point for wild type mouse lung. This dataset represents the miRNA profiling component of the study.
Project description:In order to study the gene expression changes in neonatal bronchopulmonary dysplasia (BPD) induced by hyperoxia, we used a rat model to detect the gene expression changes in the control group (A) and hyperoxia group (O) after birth.
Project description:We performed miRNA and mRNA profiling at postnatal day 14 and day 29 to compare hyperoxia-induced bronchopulmonary dysplasia and wild type. We built potential miRNA-mRNA interaction networks specific to brochopulmonary dysplasia.
Project description:We performed miRNA and mRNA profiling at postnatal day 14 and day 29 to compare hyperoxia-induced bronchopulmonary dysplasia and wild type. We built potential miRNA-mRNA interaction networks specific to brochopulmonary dysplasia.
Project description:Current techniques to diagnose and/or monitor critically ill neonates with bronchopulmonary dysplasia (BPD) require invasive sampling of body fluids, which can affect the health status of these frail neonate. We tested our hypotheses 1) it is feasible to use early urine samples from extremely low gestational age newborns at risk for bronchopulmonary dysplasia for proteomics, and 2) urine proteomics can confirm previously identified proteins and biomarkers associated with BPD without invasive sample collection. We developed a robust high throughput urine proteomics methodology that requires only 50 microliters of urine. We validated the methodology on urine collected within 72 hours of birth. Urine samples were collected from extremely low gestational age newborns (ELGANS) (gestational age (26 + 1.2) weeks) admitted to a single Neonatal Intensive Care Unit(NICU); half of whom eventually developed BPD, while the other half served as controls. Our high throughput urine proteomics approach clearly identified several BPD-associated changes in the urine proteome recapitulating expected blood proteome changes. Interestingly, sixteen identified urinary proteins are known targets of drugs approved by the Food and Drug Administration (FDA). Urine proteomics can be used for prediction of BPD risk. In addition to identifying numerous proteins implicated in BPD pathophysiology, previously found in invasively collected blood, tracheal aspirate, and broncho-alveolar lavage, urine proteomics also suggested novel potential therapeutic targets. Ease of access to urine for sequential proteomic evaluations could also allow for longitudinal monitoring of disease progression and impact of therapeutic intervention.
Project description:Bronchopulmonary dysplasia (BPD) is the most common chronic respiratory disease in premature infants. Recent studies have highlighted the contribution of genetic factors to BPD susceptibility. Our aim was to identify the genetic variants associated to BPD, through a genomewide association study. Two discovery series were performed, using a DNA pooling-based strategy in Caucasian and black African neonates.
Project description:Bronchopulmonary dysplasia (BPD) remains the most frequent chronic lung disease among infants, which involves multifactorial pathogenesis. Necroptosis represents a caspase-independent mode of programmed cell death, and its deregulation associates with lung diseases, but the mechanisms of necroptosis during BPD are indistinct. This work was conducted for unveiling the post-transcriptional regulatory mechanisms of necroptosis in BPD.
Project description:Bronchopulmonary dysplasia (BPD) is a lung disease in premature infants characterized by impaired pulmonary development which persists into later life. While advances in neonatal care have improved survival rates of premature infants, cases of BPD haves been increased. Therapeutic options are limited for prevention and treatment. This study was designed to explore differentially expressed genes associated with BPD. Cord blood mRNA from preterm neonates that went on to develop BPD (n = 6) or not (nonBPD, n = 17) was applied to Illumina HumanHT-12 arrays, we identify differentially expressed genes associated with BPD.