COPD Airway Epithelial Cell-derived Extracellular Vesicles Spread Cellular Senescence via MicroRNA-34a.

Justine V Devulder, Jonathan R Baker, Peter S Fenwick, Lina Odqvist, Louise E Donnelly, Peter J Barnes

Imperial College London National Heart and Lung Institute, London, United Kingdom of Great Britain and Northern Ireland; [email protected] College London National Heart and Lung Institute, London, United Kingdom of Great Britain and Northern Ireland; [email protected]. · pubmed

Paper

Abstract

Chronic obstructive pulmonary disease (COPD) is associated with the acceleration of lung aging, and the accumulation of senescent cells in lung tissue. MicroRNA (miR)-34a induces senescence by suppressing the anti-aging molecule, sirtuin-1 (SIRT1). Senescent cells spread senescence to neighbouring and distant cells, favouring COPD progression and its comorbidities. Mechanisms for spreading senescence remain undetermined but may be mediated by the transfer of microRNAs in extracellular vesicles. We analysed the miRNA content of extracellular vesicles in COPD and explored their effect on cellular senescence of healthy cells. EVs were isolated from small airway epithelial cells (SAEC) from healthy donors or COPD patients. Recipient healthy SAEC were cultured with EVs and the expression of miR-34a and markers of cellular senescence, p21

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Research summary

The paper claims that extracellular vesicles derived from COPD airway epithelial cells can induce cellular senescence in healthy cells via microRNA-34a. This research is relevant as it explores mechanisms of cellular senescence, which is a key factor in aging and age-related diseases, potentially contributing to understanding the root causes of aging processes.

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