Senescence of lung mesenchymal stem cells of preterm infants by cyclic stretch and hyperoxia via p21
Judith Behnke, Maurizio J. Goetz, Lena Holzfurtner, Pauline Korte, Astrid Weiß, Tayyab Shahzad, Jochen Wilhelm, Ralph T. Schermuly, Stefano Rivetti, Saverio Bellusci, Harald Ehrhardt
2024American Journal of Physiology-Lung Cellular and Molecular Physiology8 citationsDOIOpen Access PDF
Abstract
Rarefication of lung mesenchymal stem cells (MSC) due to exposure to cyclic mechanical stretch (CMS) during mechanical ventilation with oxygen-rich gas is a hallmark of bronchopulmonary dysplasia in preterm infants, but the pathomechanistic understanding is incomplete. Our studies identify a common signaling mechanism mediated by p21 accumulation, leading to cellular senescence and cell death, most pronounced during the combined exposure with in principle reversible phenotype change depending on strength and duration of exposures.
Topics & Concepts
Hox geneHyperoxiaMesenchymal stem cellBronchopulmonary dysplasiaSenescencePhenotypeDownregulation and upregulationCell biologyStem cellBiologyMedicineLungCancer researchInternal medicineGeneticsTranscription factorGenePregnancyGestational ageNeonatal Respiratory Health ResearchCongenital Diaphragmatic Hernia StudiesEpigenetics and DNA Methylation