Lower levels of senescence in human lung mesenchymal stromal cells compared to lung fibroblasts; implications for tissue regeneration in COPD.

Marissa Wisman, Dennis Kruk, Wierd Kooistra, Irene H Heijink, Roy R Woldhuis

University of Groningen, University Medical Centre Groningen, Department of Pathology and Medical Biology, Groningen, The Netherlands.University of Groningen, University Medical Centre Groningen, Department of Pathology and Medical Biology, Groningen, The Netherlands. · pubmed

Paper

Abstract

In COPD patients, lung-tissue regenerative mechanisms are thought to be exhausted, to which cellular senescence may contribute. Lung-derived mesenchymal stem/stromal cells (LMSCs) constitute a potent supportive cell type able to self-renew and promote alveolar regeneration. We hypothesized that LMSCs are less sensitive to senescence induction in COPD than other supportive cells e.g. lung fibroblasts (LFs) and therefore more promising in regenerative strategies. We compared senescence markers in LMSCs and LFs from the same subjects with/without replicative- and stress-induced senescence. LMSCs and LFs were isolated from COPD and non-COPD lung tissue using cell-specific protocols, and expanded for multiple passages under the same culture conditions. Proliferation, SA-β-gal activity, expression of senescence markers (

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Research summary

Lung mesenchymal stromal cells are less sensitive to senescence than lung fibroblasts in COPD patients. This research is relevant as it explores cellular senescence mechanisms that could contribute to tissue regeneration, addressing a root cause of aging-related decline in lung function.

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