Giuseppe
Emeritus
[Source: PLoS ONE, full text: (LINK). Abstract, edited.]
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Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza
Dahai Zheng<SUP>1</SUP>, Gino V. Limmon<SUP>1</SUP>, Lu Yin<SUP>1</SUP>, Nicola H. N. Leung<SUP>1</SUP>, Hanry Yu<SUP>3</SUP>, Vincent T. K. Chow<SUP>4</SUP><SUP>*</SUP>, Jianzhu Chen<SUP>1</SUP><SUP>,</SUP><SUP>2</SUP><SUP>*</SUP>
<SUP></SUP>
1 Interdisciplinary Research Group in Infectious Diseases, Singapore-Massachusetts Institute of Technology Alliance for Research and Technology, Singapore, Singapore, 2 The Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America, 3 Institute of Bioengineering and Nanotechnology, Agency for Science, Technology and Research, Singapore; Department of Physiology & Mechanobiology, National University of Singapore, Singapore, 4 Human Genome Laboratory, Department of Microbiology, School of Medicine, National University of Singapore, Singapore
Abstract
The lung comprises an extensive surface of epithelia constantly exposed to environmental insults. Maintaining the integrity of the alveolar epithelia is critical for lung function and gaseous exchange. However, following severe pulmonary damage, what progenitor cells give rise to alveolar type I and II cells during the regeneration of alveolar epithelia has not been fully determined. In this study, we have investigated this issue by using transgenic mice in which Scgb1a1-expressing cells and their progeny can be genetically labeled with EGFP. We show that following severe alveolar damage induced either by bleomycin or by infection with influenza virus, the majority of the newly generated alveolar type II cells in the damaged parenchyma were labeled with EGFP. A large proportion of EGFP-expressing type I cells were also observed among the type II cells. These findings strongly suggest that Scgb1a1-expressing cells, most likely Clara cells, are a major cell type that gives rise to alveolar type I and II cells during the regeneration of alveolar epithelia in response to severe pulmonary damage in mice.
Citation: Zheng D, Limmon GV, Yin L, Leung NHN, Yu H, et al. (2012) Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza. PLoS ONE 7(10): e48451. doi:10.1371/journal.pone.0048451
Editor: Saverio Bellusci, Children's Hospital Los Angeles, United States of America
Received: August 18, 2012; Accepted: September 25, 2012; Published: October 31, 2012
Copyright: ? 2012 Zheng et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This research was supported by the National Research Foundation Singapore through the Singapore MIT Alliance for Research and Technology's Infectious Disease-IRG research programme. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: jchen@mit.edu (JC); vincent_chow@nuhs.edu.sg (VC)
-Dahai Zheng<SUP>1</SUP>, Gino V. Limmon<SUP>1</SUP>, Lu Yin<SUP>1</SUP>, Nicola H. N. Leung<SUP>1</SUP>, Hanry Yu<SUP>3</SUP>, Vincent T. K. Chow<SUP>4</SUP><SUP>*</SUP>, Jianzhu Chen<SUP>1</SUP><SUP>,</SUP><SUP>2</SUP><SUP>*</SUP>
<SUP></SUP>
1 Interdisciplinary Research Group in Infectious Diseases, Singapore-Massachusetts Institute of Technology Alliance for Research and Technology, Singapore, Singapore, 2 The Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America, 3 Institute of Bioengineering and Nanotechnology, Agency for Science, Technology and Research, Singapore; Department of Physiology & Mechanobiology, National University of Singapore, Singapore, 4 Human Genome Laboratory, Department of Microbiology, School of Medicine, National University of Singapore, Singapore
Abstract
The lung comprises an extensive surface of epithelia constantly exposed to environmental insults. Maintaining the integrity of the alveolar epithelia is critical for lung function and gaseous exchange. However, following severe pulmonary damage, what progenitor cells give rise to alveolar type I and II cells during the regeneration of alveolar epithelia has not been fully determined. In this study, we have investigated this issue by using transgenic mice in which Scgb1a1-expressing cells and their progeny can be genetically labeled with EGFP. We show that following severe alveolar damage induced either by bleomycin or by infection with influenza virus, the majority of the newly generated alveolar type II cells in the damaged parenchyma were labeled with EGFP. A large proportion of EGFP-expressing type I cells were also observed among the type II cells. These findings strongly suggest that Scgb1a1-expressing cells, most likely Clara cells, are a major cell type that gives rise to alveolar type I and II cells during the regeneration of alveolar epithelia in response to severe pulmonary damage in mice.
Citation: Zheng D, Limmon GV, Yin L, Leung NHN, Yu H, et al. (2012) Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza. PLoS ONE 7(10): e48451. doi:10.1371/journal.pone.0048451
Editor: Saverio Bellusci, Children's Hospital Los Angeles, United States of America
Received: August 18, 2012; Accepted: September 25, 2012; Published: October 31, 2012
Copyright: ? 2012 Zheng et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This research was supported by the National Research Foundation Singapore through the Singapore MIT Alliance for Research and Technology's Infectious Disease-IRG research programme. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: jchen@mit.edu (JC); vincent_chow@nuhs.edu.sg (VC)
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