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Cord blood gene expression profiles of bronchopulmonary dysplasia in preterm infants

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE188944 | GEO | 2022/05/05

REPOSITORIES: GEO

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Cord blood methylation 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 the relationship between gestational age (GA), birth weight and estímate blood cell-type composition in premature infants and to elucidate early epigenetic biomarkers associated with BPD. Cord blood DNA from preterm neonates that went on to develop BPD (n = 14) or not (nonBPD, n = 93) was applied to Illumina 450K methylation arrays. Using DNA methylation analysis of cord blood DNA, we investigated association of GA and birth weight with the estimated distribution of cord blood cell types, particularly the nucleated red blood cell (NRBC) in a pilot-size cohort of preterm infants with or without BPD. We describe changes in methylation-based estimates of blood cell-type composition in relation to GA and birth weight. After adjusting for covariates (GA, birth weight, cell type proportions, etc.) we identify differentially methylated CpGs and genes associated with BPD.

2022-05-05 | GSE188949 | GEO

Epigenome-wide association study on peripheral blood DNA 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 the relationship between gestational age (GA), birth weight and estímate blood cell-type composition in premature infants and to elucidate early epigenetic biomarkers associated with BPD. Peripheral blood DNA (at days 14 and 28) from preterm neonates that went on to develop BPD (n = 14) or not (nonBPD, n = 93) was applied to Illumina EPIC methylation arrays. Using DNA methylation analysis of cord blood DNA, we investigated association of GA and birth weight with the estimated distribution of cord blood cell types, particularly the nucleated red blood cell (NRBC) in a pilot-size cohort of preterm infants with or without BPD. We describe changes in methylation-based estimates of blood cell-type composition in relation to GA and birth weight. After adjusting for covariates (GA, birth weight, cell type proportions, etc.) we identify differentially methylated CpGs and genes associated with BPD at different time points.

2023-07-05 | GSE225313 | GEO

A genomewide association study for bronchopulmonary dysplasia using DNA pooling

2011-11-22 | GSE22284 | GEO

Umbilical Cord Blood-derived Exosomes from Very Preterm Infants with Bronchopulmonary Dysplasia Impaired Endothelial Angiogenesis: Roles of Exosomal MicroRNAs

Project description:Premature infants have a high risk of bronchopulmonary dysplasia (BPD), which is characterized by abnormal development of alveoli and pulmonary vessels. Exosomes and exosomal miRNAs (EXO-miRNAs) from bronchoalveolar lavage fluid are involved in the development of BPD and might serve as predictive biomarkers for BPD. However, the roles of exosomes and EXO-miRNAs from umbilical cord blood of BPD infants in regulating angiogenesis are yet to be elucidated. In this study, we showed that umbilical cord blood-derived exosomes from BPD infants impaired angiogenesis in vitro. Next generation sequencing of EXO-miRNAs from preterm infants without (NBPD group) or with BPD (BPD group) uncovered a total of 418 differentially expressed (DE) EXO-miRNAs. These DE EXO-miRNAs were primarily enriched in cellular function-associated pathways including the PI3K/Akt and angiogenesis- related signaling pathways. Among those EXO-miRNAs which are associated with PI3K/Akt and angiogenesis-related signaling pathways, BPD reduced expression of hsa-miR-103a-3p and hsa-miR-185-5p exhibiting most significant reduction (14.3% and 23.1% of NBPD group, respectively); BPD increased hsa-miR-200a-3p expression by 2.64 folds of NBPD group. Furthermore, overexpression of hsa-miR-103a-3p and hsa-miR-185-5p in normal human umbilical vein endothelial cells (HUVECs) significantly enhanced endothelial cell proliferation, tube formation and cell migration, whereas overexpressing hsa-miR-200a-3p inhibited these cellular responses. This study demonstrates that exosomes derived from umbilical cord blood of BPD infants impair angiogenesis, possibly via DE EXO-miRNAs, which might contribute to the development of BPD.

2021-02-16 | GSE166762 | GEO

Early Angiogenic Proteins Associated with High Risk for Bronchopulmonary Dysplasia and Pulmonary Hypertension in Preterm Infants

Project description:Introduction: Early pulmonary vascular disease in preterm infants is associated with the subsequent development of bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH), however, mechanisms that contribute to or identify infants with increased susceptibility for BPD and/or PH are incompletely understood. Therefore, we tested if changes in circulating angiogenic peptides during the first week of life are associated with the later development of BPD and/or PH. We further sought to determine alternate peptides and related signalling pathways with the risk for BPD or PH. Methods: We prospectively enrolled infants with gestational age <34 weeks gestation and collected blood samples during their first week of life. BPD and PH were assessed at 36 weeks postmenstrual age. Samples were assayed for each of the 1121 peptides included in the SOMAscanTM technology, with subsequent pathway analysis. Results: Of 102 study infants, 82 had BPD and 13 had PH. Multiple angiogenic proteins (PF-4, VEGF121, ANG-1, BMP10, HGF, ANG2) were associated with the subsequent diagnosis of BPD, and FGF-19, PF-4, CTAP-III and PDGF-AA levels were associated with BPD severity. Early increases in BMP10 was strongly associated with the late risk for BPD and PH. Conclusion: We found that early alterations of circulating angiogenic peptides and others were associated with the subsequent development of BPD. We further identified peptides that were associated with BPD severity and BPD-associated PH, including BMP10. We speculate that proteomic biomarkers during the first week of life may identify infants at risk for BPD and/or PH to enhance care and research.

2020-01-15 | GSE121097 | GEO

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. DNA pooling studies were performed in two discovery series. The first discovery series was made up of 22 Caucasian infants with BPD and 76 Caucasian controls. The second discovery series was composed of 21 black African infants with BPD and 86 black African controls. Equimolar amounts of each DNA sample were then added to either the case or control pool, for each series. To control for experimental errors, several independent sets of pools were constructed. Concerning the Caucasian series, 3 sets of identical pools were constructed with one made in double quantity in order to hybridize it twice, which led to 4 independent replicates. Concerning the black African series, 4 sets of identical pools were constructed and each was hybridized once, leading also to 4 independent replicates. Genotyping was performed using the Infinium II Illumina HumanHap300 Genotyping BeadChip array for the Caucasian population and the Illumina HumanHap650Y array for the black African population. Each replicate was hybridized once which led to 4 arrays for each case and control pools and for each population. A total of 16 arrays were performed. technical replicate: Sample 1, Sample 2, Sample 3, Sample 4 technical replicate: Sample 5, Sample 6, Sample 7, Sample 8 technical replicate: Sample 9, Sample 10, Sample 11, Sample 12 technical replicate: Sample 13, Sample 14, Sample 15, Sample 16

2011-11-22 | E-GEOD-22284 | biostudies-arrayexpress

Leveraging Integrated RNA Sequencing to Decipher Adrenomedullin’s Protective Mechanisms in Experimental Bronchopulmonary Dysplasia

Project description:Bronchopulmonary dysplasia (BPD) is a chronic lung disease commonly affecting premature infants, with limited therapeutic options and increased long-term consequences. Adrenomedullin (Adm), a proangiogenic peptide hormone, has been found to protect rodents against experimental BPD. This study aims to elucidate the molecular and cellular mechanisms through which Adm influences BPD pathogenesis using a lipopolysaccharide (LPS)-induced model of experimental BPD in mice. Bulk RNA sequencing of Adm-sufficient (wild-type or Adm+/+) and Adm-haplodeficient (Adm+/-) mice lungs, integrated with single-cell RNA sequencing data, revealed distinct gene expression patterns and cell type alterations associated with Adm deficiency and LPS exposure. Notably, computational integration with cell atlas data revealed that Adm-haplodeficient mouse lungs exhibited gene expression signatures characteristic of increased inflammation, natural killer (NK) cell frequency and decreased endothelial cell and type II pneumocyte frequency. Furthermore, in silico human BPD patient data analysis supported our cell type frequency finding, highlighting elevated NK cells in BPD infants. These results underscore the protective role of Adm in experimental BPD and emphasize that it is a potential therapeutic target for BPD infants with an inflammatory phenotype.

2024-06-17 | GSE264612 | GEO

RNA-Seq of blood in preterm infants with Bronchopulmonary dysplasia.

Project description:RNA-Seq of peripheral blood at 36 weeks post-menstrual age, the time BPD was diagnosed. Using this we identified more than 400 genes that were significantly changed in BPD infants compared to controls.

2019-10-04 | GSE125873 | GEO

RNA-seq of peripheral whole blood from ten healthy preterm infants and ten preterm infants with bronchopulmonary dysplasia

Project description:We procured peripheral whole blood from ten healthy preterm infants and ten preterm infants with bronchopulmonary dysplasia

2024-10-27 | E-MTAB-14506 | biostudies-arrayexpress

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

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