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Molecular Mechanism of Oncostatin M-Mediated Bronchopulmonary Dysplasia Induced by Intrauterine Inflammation

ABSTRACT: Intrauterine inflammation is a key risk factor for bronchopulmonary dysplasia (BPD) in preterm infants, though mechanisms remain unclear. We found that intrauterine inflammation activates fetal pulmonary macrophages, which upregulate Oncostatin M (OSM) via Junb. OSM then induces alveolar epithelial cell senescence through the Atf3-p21 signaling pathway, resulting in developmental lung injury. This study identifies a novel macrophage-OSM-epithelial senescence axis in BPD pathogenesis, offering potential therapeutic targets.

ORGANISM(S): Mus musculus

PROVIDER: GSE310065 | GEO | 2026/09/16

REPOSITORIES: GEO

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Molecular Mechanism of Oncostatin M-Mediated Bronchopulmonary Dysplasia Induced by Intrauterine Inflammation [scRNA-seq]

Project description:Intrauterine inflammation is a key risk factor for bronchopulmonary dysplasia (BPD) in preterm infants, though mechanisms remain unclear. We found that intrauterine inflammation activates fetal pulmonary macrophages, which upregulate Oncostatin M (OSM) via Junb. OSM then induces alveolar epithelial cell senescence through the Atf3-p21 signaling pathway, resulting in developmental lung injury. This study identifies a novel macrophage-OSM-epithelial senescence axis in BPD pathogenesis, offering potential therapeutic targets.

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CELLULAR SENESCENCE CONTRIBUTES TO THE PROGRESSION OF HYPEROXIC BRONCHOPULMONARY DYSPLASIA

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NR4A1 Mediates Offspring Bronchopulmonary Dysplasia-Like Lung Injury Induced by Intrauterine Inflammation in Mice

Project description:Background Intrauterine inflammation (IUI) is involved in the development of bronchopulmonary dysplasia (BPD). Previously, we observed BPD-like pathological changes in a mouse model of IUI. Here, we aimed to investigate key molecules involved in IUI-induced neonatal lung injury along with the long-term outcomes. Methods Pregnant C57BL/6 mice were randomly divided into control and IUI groups. Lung injury was evaluated using hematoxylin-eosin and Masson's trichrome staining. An NR4A1 overexpression plasmid was used to explore the downstream molecules acting in vitro. Accordingly, IUI-induced lung injury intervention was verified using Nr4a1 siRNA. Results The lungs of IUI-induced offspring showed a simple structure from postnatal day 1 to 6 months, with increased pulmonary fibrosis from 3 to 6 months postnatal. Postnatal NR4A1 intervention reversed IUI-induced neonatal lung injury. NR4A1 overexpression decreased cell proliferation and influenced the expression of epithelial-mesenchymal transition (EMT)-related key genes in MLE-12 cells. EREG is a downstream target of NR4A1, and blocking the receptor of EREG would recover the expression of EMT-related genes. Conclusion IUI induced BPD-like lung injury in neonates and pulmonary fibrosis in adults. The NR4A1-EREG-EGFR signaling pathway in pulmonary epithelial cells plays an important role in IUI-induced lung injury in offspring.

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2022-04-04 | PXD028895 | Pride

The interleukin 22–oncostatin M axis promotes intestinal inflammation and tumorigenesis

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