Role of mesenchymal cell death in lung remodeling after injury

Vitaly A Polunovsky, Baruch Chen, Craig A Henke, Dale Snover, Christine H Wendt, David H Ingbar, Peter B Bitterman

Research output: Contribution to journalArticlepeer-review

192 Scopus citations


Repair after acute lung injury requires elimination of granulation tissue from the alveolar airspace. We hypothesized that during lung repair, signals capable of inducing the death of the two principal cellular elements of granulation tissue, fibreblasts and endothelial cells, would be present at the air-lung interface. Bronchoalveolar lavage fluid obtained from patients during lung repair induced both fibroblast and endothelial cell death, while fluid obtained at the time of injury or from patient controls did not. The mode of cell death for endothelial cells was apoptosis. Fibroblast death, while morphologically distinct from necrosis, also differed from typical apoptosis. Only proliferating cells were susceptible to the bioactivities in lavage fluid, which were trypsin sensitive and lipid insoluble. Histological examination of lung tissue from patients after lung injury revealed evidence of apoptotic cells within airspace granulation tissue. Our results suggest that cell death induced by peptide(s) present at the air-lung interface may participate in the remodeling process that accompanies tissue repair after injury.

Original languageEnglish (US)
Pages (from-to)388-397
Number of pages10
JournalJournal of Clinical Investigation
Issue number1
StatePublished - Jul 1993


  • Apoptosis
  • Cell death
  • Endothelial cells
  • Fibroblasts
  • Granulation tissue

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