Role of mesenchymal cell death in lung remodeling after injury.

V A Polunovsky; B Chen; C Henke; D Snover; C Wendt; D H Ingbar; P B Bitterman

doi:10.1172/JCI116578

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

Find articles by Polunovsky, V. in: PubMed | Google Scholar

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

Find articles by Chen, B. in: PubMed | Google Scholar

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

Find articles by Henke, C. in: PubMed | Google Scholar

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

Find articles by Snover, D. in: PubMed | Google Scholar

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

Find articles by Wendt, C. in: PubMed | Google Scholar

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

Find articles by Ingbar, D. in: PubMed | Google Scholar

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

Find articles by Bitterman, P. in: PubMed | Google Scholar

Published in Volume 92, Issue 1 on July 1, 1993
J Clin Invest. 1993;92(1):388–397. https://doi.org/10.1172/JCI116578.
© 1993 The American Society for Clinical Investigation

Published July 1, 1993 - Version history

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, fibroblasts 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.

Images.