Telomerase Prevents Emphysema in Old Mice by Sustaining Subpopulations of Endothelial and AT2 Cells
BREAU, M.; CAYROU, C.; CHURIKOV, D.; FOUILLADE, C.; CURRAS ALONSO, S.; BAUWENS, S.; JOURQUIN, F.; BRAUD, L.; FIORE, F.; CATELLANO, R.; JOSSELIN, E.; SANCHEZ-FERRER, C.; GIOVINAZZO, G.; GILSON, E.; FLORES, I.; LONDONO-VALLEJO, A.; ADNOT, S.; GELI, V.
Show abstract
Accumulation of senescent cells has been causally linked to the development of age-related pathologies. Here, we characterized a new mouse model (p21+/Tert) whose telomerase (TERT) is expressed from the p21 promoter that can be activated in response to telomere dysfunction. Lung parenchyma from p21+/Tert old mice accumulated fewer senescent cells with age and this correlated with a reduction in age-related alveolar space enlargement, a feature of pulmonary emphysema. This protection against emphysema depends on TERT catalytic activity and is associated with increased proliferation of pulmonary endothelial cells (EC) and capillary density. Single-cell RNA sequencing of lung cells revealed that TERT expression was associated with the enrichment of ECs expressing genes involved in vessel regeneration and in AT2 cells overexpressing S/G2M markers. These findings indicate that p21-promoter-dependent expression of catalytically active telomerase prevents emphysema by sustaining the proliferation of subclasses of EC and AT2 cells.
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