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Cellular senescence in hyperoxic neonatal rat lung

ABSTRACT: Cellular senescence in hyperoxic neonatal rat lung

PROVIDER: PRJNA1013085 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25915522.fastq.gz	Fastqsanger.gz
	SRR25915523.fastq.gz	Fastqsanger.gz
	SRR25915524.fastq.gz	Fastqsanger.gz
	SRR25915525.fastq.gz	Fastqsanger.gz
	SRR25915526.fastq.gz	Fastqsanger.gz

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Cellular senescence in hyperoxic neonatal rat lung

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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.

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