ArticleAmerican journal of physiology. Lung cellular and molecular physiology2024
Senescence of lung mesenchymal stem cells of preterm infants by cyclic stretch and hyperoxia via p21.
Article in American journal of physiology. Lung cellular and molecular physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Mesenchymal Stem Cell (MSC)-based therapies for neonatal lung and brain injury - one size fits all?Molecular and cellular pediatrics · 2026Review
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Preventive application of lung growth factors and lack of attenuation of phenotype disruption of lung resident MSC from preterm infants by hyperoxia.Molecular and cellular pediatrics · 2026Article
- Observational
- Hyperoxia promotes bronchopulmonary dysplasia via Noggin-mediated BMP4 antagonism and cellular senescence.Frontiers in physiology · 2026Article
- Phenotype disruption of umbilical cord derived MSC by cyclic mechanical stretch and hyperoxia mediated by p21.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Phenotype distortion of lung resident mesenchymal stem cells (MSC) in preterm infants is a hallmark event in the pathogenesis of bronchopulmonary dysplasia (BPD). Here, we evaluated the impact of cyclic mechanical stretch (CMS) and hyperoxia (HOX). The negative action of HOX on proliferation and cell death was more pronounced at 80% than at 40%. Although the impact of CMS alone was modest, CMS plus HOX displayed the strongest effect sizes. Exposure to CMS and/or HOX induced the downregulation of PDGFRα, and cellular senescence preceded by p21 accumulation. p21 interference interfered with cellular senescence and resulted in aggravated cell death, arguing for a prosurvival mechanism. HOX 40% and limited exposure to HOX 80% prevailed in a reversible phenotype with reuptake of proliferation, while prolonged exposure to HOX 80% resulted in definite MSC growth arrest. Our mechanistic data explain how HOX and CMS induce the effects on MSC phenotype disruption. The results are congruent with the clinical observation that preterm infants requiring supplemental oxygen plus mechanical ventilation are at particular risk for BPD. Although inhibiting p21 is not a feasible approach, limiting the duration and magnitude of the exposures is promising.
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Registered trials
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