Effect of hyperoxic exposure on neonatal lung cDCs expression
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ABSTRACT:
PROVIDER: PRJNA927310 | ENA |
REPOSITORIES: ENA
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Project description:Bronchopulmonary dysplasia (BPD), a chronic pulmonary sequela of preterm birth, increases susceptibility to respiratory viral infection. Exposure to hyperoxia of neontal mice (a model of BPD) increases the number of activated, IL-12 producing lung CD103+ dendritic cells (DCs) and augments the inflammatory response to rhinovirus infection. We used microarray analysis to detail the effect of hyperoxia on the gene expression of the two main subsets of lung cDC, including CD103+ DCs and CD11bhi DC. We identified distinct up- and down-regulated genes in response to hyperoxia in both cDC subclasses.
2023-02-02 | GSE223701 | GEO
Project description:Growth Differentiation Factor 15 (GDF15) is a divergent member of the TGF-β superfamily, and its expression increases under various stress conditions, including inflammation, hyperoxia, and senescence. GDF15 expression is increased in neonatal murine BPD models, and GDF15 loss exacerbates oxidative stress and decreases viability in vitro in pulmonary epithelial and endothelial cells. Our overall hypothesis is that the loss of GDF15 will exacerbate hyperoxic lung injury in the neonatal lung in vivo. We exposed neonatal Gdf15-/- mice and wild-type (WT) controls on a similar background to room air or hyperoxia (95% O2) for 5 days after birth. The mice were euthanized on PND 21. Gdf15 -/- mice had higher mortality and lower body weight than WT mice after exposure to hyperoxia. Upon exposure to hyperoxia, female mice had higher alveolar simplification in the Gdf15-/- group than the female WT group. Gdf15-/- and WT mice showed no difference in the degree of the arrest in angiogenesis upon exposure to hyperoxia. Gdf15-/- mice showed lower macrophage count in the lungs compared to WT mice. Our results suggest that Gdf15 deficiency decreases the tolerance to hyperoxic lung injury with evidence of sex-specific differences.
2023-07-20 | GSE211744 | GEO
Project description:Cellular senescence in hyperoxic neonatal rat lung
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Project description:Role of Gdf15 in neonatal hyperoxic lung injury
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Project description:Bronchopulmonary dysplasia (BPD) is characterized by an arrest in alveolarization, abnormal vascular development and variable interstitial fibroproliferation in the premature lung. Endothelial to mesenchymal transition (Endo-MT) may be a source of pathologic fibrosis in many organ systems. Whether Endo-MT contributes to the pathogenesis of BPD is not known. We tested the hypothesis that pulmonary endothelial cells will show increased expression of Endo-MT markers upon exposure to hyperoxia and that sex as a biological variable will modulate differences in expression. WT and Cdh5-PAC CreERT2 (endothelial reporter) neonatal male and female mice (C57BL6) were exposed to hyperoxia (0.95 FiO2) either during the saccular stage of lung development (95% FiO2; PND1-5) or through the saccular and early alveolar stages of lung development (75% FiO2; PND1-14). Expression of Endo-MT markers were measured in whole lung and endothelial cell mRNA. Sorted lung endothelial cells were subjected to bulk RNA-Seq. We show that exposure of the neonatal lung to hyperoxia leads to upregulation of key markers of EndoMT Neonatal male mice show higher expression of genes related to EndoMT. Furthermore, using lung sc-RNAseq data from neonatal lung we were able to show that xxx. Markers related to Endo-MT are upregulated in the neonatal lung upon exposure to hyperoxia and show sex-specific differences. Mechanisms mediating EndoMT in the injured neonatal lung can modulate the response of the neonatal lung to hyperoxic injury and need further investigation.
2023-11-08 | GSE230672 | GEO
Project description:Sex chromosomes versus gonadal hormones in neonatal hyperoxic lung injury
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Project description:Pulmonary vascular development is essential for alveolarization, and disruption of this process contributes to bronchopulmonary dysplasia (BPD) pulmonary pathology. Proper vascular development requires an orchestration of many cell types within the lung. However, the mechanisms by which pericytes support the endothelium in the postnatal lung remain poorly understood. Here, we identify FOXF2 as a critical transcription factor that governs pericyte maturation and function during postnatal lung development and regeneration. FOXF2 expression in pericytes increases postnatally and is selectively downregulated following neonatal hyperoxic injury. Pdgfrb-CreER mediated Foxf2 deletion in pericytes leads to pericyte hyperplasia, impaired migration, reduced expression of angiogenic factors such as ANGPTL4, and exacerbated alveolar simplification in a neonatal murine model of BPD. Transcriptomic and genomic studies demonstrate that FOXF2 maintains chromatin accessibility at pro-angiogenic loci and modulates paracrine signaling essential for endothelial regeneration. Loss of FOXF2 disrupts pericyte–endothelial crosstalk, impairing angiogenesis and alveolar repair during injury. Our study identifies FOXF2 as a central transcriptional regulator of pericyte-driven vascular niche function in the neonatal lung and underscores the pathogenic role of dysfunctional pericytes in BPD.
2025-12-31 | GSE297570 | GEO
Project description:Pulmonary vascular development is essential for alveolarization, and disruption of this process contributes to bronchopulmonary dysplasia (BPD) pulmonary pathology. Proper vascular development requires an orchestration of many cell types within the lung. However, the mechanisms by which pericytes support the endothelium in the postnatal lung remain poorly understood. Here, we identify FOXF2 as a critical transcription factor that governs pericyte maturation and function during postnatal lung development and regeneration. FOXF2 expression in pericytes increases postnatally and is selectively downregulated following neonatal hyperoxic injury. Pdgfrb-CreER mediated Foxf2 deletion in pericytes leads to pericyte hyperplasia, impaired migration, reduced expression of angiogenic factors such as ANGPTL4, and exacerbated alveolar simplification in a neonatal murine model of BPD. Transcriptomic and genomic studies demonstrate that FOXF2 maintains chromatin accessibility at pro-angiogenic loci and modulates paracrine signaling essential for endothelial regeneration. Loss of FOXF2 disrupts pericyte–endothelial crosstalk, impairing angiogenesis and alveolar repair during injury. Our study identifies FOXF2 as a central transcriptional regulator of pericyte-driven vascular niche function in the neonatal lung and underscores the pathogenic role of dysfunctional pericytes in BPD.
2025-12-31 | GSE297575 | GEO
Project description:Pulmonary vascular development is essential for alveolarization, and disruption of this process contributes to bronchopulmonary dysplasia (BPD) pulmonary pathology. Proper vascular development requires an orchestration of many cell types within the lung. However, the mechanisms by which pericytes support the endothelium in the postnatal lung remain poorly understood. Here, we identify FOXF2 as a critical transcription factor that governs pericyte maturation and function during postnatal lung development and regeneration. FOXF2 expression in pericytes increases postnatally and is selectively downregulated following neonatal hyperoxic injury. Pdgfrb-CreER mediated Foxf2 deletion in pericytes leads to pericyte hyperplasia, impaired migration, reduced expression of angiogenic factors such as ANGPTL4, and exacerbated alveolar simplification in a neonatal murine model of BPD. Transcriptomic and genomic studies demonstrate that FOXF2 maintains chromatin accessibility at pro-angiogenic loci and modulates paracrine signaling essential for endothelial regeneration. Loss of FOXF2 disrupts pericyte–endothelial crosstalk, impairing angiogenesis and alveolar repair during injury. Our study identifies FOXF2 as a central transcriptional regulator of pericyte-driven vascular niche function in the neonatal lung and underscores the pathogenic role of dysfunctional pericytes in BPD.
2025-12-31 | GSE297573 | GEO
Project description:Sex-specific differences in the pulmonary epigenome in neonatal hyperoxic lung injury
| PRJNA623915 | ENA