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PLoS One. 2017 May 19;12(5):e0177921. doi: 10.1371/journal.pone.0177921. eCollection 2017.

Evidence for pleural epithelial-mesenchymal transition in murine compensatory lung growth.

Author information

1
Laboratory of Adaptive and Regenerative Biology, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
2
Institute of Functional and Clinical Anatomy, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
3
Molecular and Integrative Physiological Sciences, Harvard School of Public Health, Boston, Massachusetts, United States of America.

Abstract

In many mammals, including rodents and humans, removal of one lung results in the compensatory growth of the remaining lung; however, the mechanism of compensatory lung growth is unknown. Here, we investigated the changes in morphology and phenotype of pleural cells after pneumonectomy. Between days 1 and 3 after pneumonectomy, cells expressing α-smooth muscle actin (SMA), a cytoplasmic marker of myofibroblasts, were significantly increased in the pleura compared to surgical controls (p < .01). Scanning electron microscopy of the pleural surface 3 days post-pneumonectomy demonstrated regions of the pleura with morphologic features consistent with epithelial-mesenchymal transition (EMT); namely, cells with disrupted intercellular junctions and an acquired mesenchymal (rounded and fusiform) morphotype. To detect the migration of the transitional pleural cells into the lung, a biotin tracer was used to label the pleural mesothelial cells at the time of surgery. By post-operative day 3, image cytometry of post-pneumonectomy subpleural alveoli demonstrated a 40-fold increase in biotin+ cells relative to pneumonectomy-plus-plombage controls (p < .01). Suggesting a similar origin in space and time, the distribution of cells expressing biotin, SMA, or vimentin demonstrated a strong spatial autocorrelation in the subpleural lung (p < .001). We conclude that post-pneumonectomy compensatory lung growth involves EMT with the migration of transitional mesothelial cells into subpleural alveoli.

PMID:
28542402
PMCID:
PMC5438137
DOI:
10.1371/journal.pone.0177921
[Indexed for MEDLINE]
Free PMC Article

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