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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human low gestational age newborns as predictors of bronchopleural pulmonary dysplasia

ABSTRACT: One third to one half of all infants born before the 28th wek of gestation develop BPD bronchopulmonary dysplasia. Our objective is to evaluate the feasibility of using expression profiling in umbilical cord tissue to discover molecular signatures for developmental staging and for risk of BPD. Experiment Overall Design: 54 samples, no replicates

ORGANISM(S): Homo sapiens

SUBMITTER: Jennifer Cohen

PROVIDER: E-GEOD-8586 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Perturbation of gene expression of the chromatin remodeling pathway in premature newborns at risk for bronchopulmonary dysplasia.

Cohen Jennifer J Van Marter Linda J LJ Sun Yao Y Allred Elizabeth E Leviton Alan A Kohane Isaac S IS

Genome biology 20070101 10

<h4>Background</h4>One-third to one-half of all infants born before the 28th week of gestation develop bronchopulmonary dysplasia (BPD). Inflammatory regulators appear to be involved in the pathogenesis of BPD, possibly beginning in fetal life. To evaluate the feasibility of using expression profiling in umbilical cord tissue to discover molecular signatures for developmental staging and for determining risk of BPD, we conducted a cross-sectional study of infants born at less than 28 weeks of ge ...[more]

PMID: 17916252

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Expression profiles of extremely low gestational age newborns as predictors of BPD

Project description:One third to one half of all infants born before the 28th wek of gestation develop BPD bronchopulmonary dysplasia. Our objective is to evaluate the feasibility of using expression profiling in umbilical cord tissue to discover molecular signatures for developmental staging and for risk of BPD. Keywords: disease state analysis

2007-07-26 | GSE8586 | GEO

Urine Proteomics for Noninvasive Monitoring of Biomarkers in Bronchopulmonary 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.

2022-04-04 | PXD028895 | Pride

A genomewide association study for bronchopulmonary dysplasia using DNA pooling

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.

2011-11-22 | GSE22284 | GEO

Post-transcriptional regulation of necroptosis gene EIF2AK2 in peripheral blood of bronchopulmonary dysplasia

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.

2024-02-21 | GSE219156 | GEO

Cord blood gene expression profiles of bronchopulmonary dysplasia in preterm infants

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.

2022-05-05 | GSE188944 | GEO

Identification of Novel Biomarkers of Bronchopulmonary Dysplasia model

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.

2022-08-29 | GSE212098 | GEO

Oxygen induced complication of prematurity: from experimental data to prevention strategy

Project description:A prospective study was conducted in the Neonatal Intensive Care Unit of the University Children's hospital between September 1, 2008 and November 30, 2010. The entry criteria were (1) preterm birth below 32 weeks gestational age, (2) birthweight<1500g (VLBW). During the follow-up period, bronchopulmonary dysplasia (BPD) was diagnosed in 68 (61%) infants, including 40 (36%) children with mild disease, 13 (12%) with moderate and 15 (13%) with severe BPD. Forty-three babies served as a control group (no BPD). One hundred twenty newborns were included at the start of the study. Three blood samples (0.3 ml) were drawn from all the study participants for microarray assessment of gene expression profiles around the 5th, 14th and 28th days of life. Note that microarrays were not taken for all patients at all time points (A,B,C).

2011-11-01 | E-GEOD-32472 | biostudies-arrayexpress

Different expression profiles of lncRNA, mRNA and circRNA in peripheral blood (ceRNA) of normal newborns and children with BPD.

Project description:Increasing evidence shows that circular RNAs (circRNAs) play a vital role in the development of various diseases. A recent sequencing analysis of peripheral blood of bronchopulmonary dysplasia (BPD) patients showed that circABCC4 expression was significantly up-regulated. However, the specific function and potential mechanism of circRNAs in BPD remain unclear.

2021-09-30 | GSE158423 | GEO

Proteome analysis of a human donor cohort to study bronchopulmonary dysplasia

Project description:Bronchopulmonary Dysplasia (BPD) is a disease of prematurity related to the arrest of normal lung development. The objective of this study was to perform whole lung proteomics to identify proteins and pathways differentially regulated in BPD in early childhood. The proteomes of biopsies from pediatric human donors aged 1.3 to 3 years were classified based on history of prematurity and histopathologic severity of "Healed" BPD [hBPD] (N=3) and "Established" BPD [eBPD] (N=3) with respective full term age-matched controls (N=6). Samples were analyzed using aTMT16plex labelling strategy. Code employed to perform the statistics is available at https://github.com/GeremyClair/Proteome_analysis_of_a_human_donor_cohort_to_study_bronchiopulmonary_displasia

2023-03-15 | MSV000091493 | MassIVE

CELLULAR SENESCENCE CONTRIBUTES TO THE PROGRESSION OF HYPEROXIC BRONCHOPULMONARY DYSPLASIA

Project description:Oxidative stress (OS), inflammation, and endoplasmic reticulum (ER) stress sequentially occur in the rat model of hyperoxia (HOX) induced bronchopulmonary dysplasia (BPD), and they all increase DNA damage. Tumor suppressors increase after DNA damage, followed by apoptosis or cellular senescence when the damage becomes irreparable. Although cellular senescence contributes to wound healing, its persistence will inhibit growth potential. Therefore, we hypothesized that the persistence of cellular senescence plays a role in BPD progression. We detected evidence of increased cellular senescence in rat and human BPD lungs. Foxo4-p53 binding was increased in BPD rat lungs, and inhibition of this binding attenuated BPD severity, indicating that such binding contributes to BPD's cellular senescence. Treatment with tauroursodeoxycholic acid (TUDCA) decreases ER stress. N-Acetyl-lysyltyrosylcysteine-amide (KYC) reduced toxic oxidant production by myeloperoxidase (MPO) and subsequent OS and inflammation. Both agents effectively decreased cellular senescence. Concomitantly, alveolar complexity and the number of type 2 alveolar cells increased, indicating that MPO-mediated OS and ER stress preceded cellular senescence in BPD rat pup lungs. These data suggest that cellular senescence plays an essential role in BPD progression. Reducing MPO toxic oxidant production, ER stress, and attenuating cellular senescence are potential therapeutic strategies for halting BPD progression. Using multiomic data to investigate the role of cellular senescence in the development of BPD in rat model.

2024-01-01 | GSE223745 | GEO

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