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10.1371/journal.pone.0177921

http://scihub22266oqcxt.onion/10.1371/journal.pone.0177921
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C5438137!5438137!28542402
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suck abstract from ncbi


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pmid28542402      PLoS+One 2017 ; 12 (5): ä
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  • Evidence for pleural epithelial-mesenchymal transition in murine compensatory lung growth #MMPMID28542402
  • Ysasi AB; Wagner WL; Valenzuela CD; Kienzle A; Servais AB; Bennett RD; Tsuda A; Ackermann M; Mentzer SJ
  • PLoS One 2017[]; 12 (5): ä PMID28542402show ga
  • 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 ?-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.
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