Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza
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...
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| Format: | Article |
| Language: | en_US |
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Public Library of Science
2013
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| Online Access: | http://hdl.handle.net/1721.1/76658 https://orcid.org/0000-0002-5687-6154 |
| _version_ | 1826206253235306496 |
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| author | Zheng, Dahai Limmon, Gino V. Yin, Lu Leung, Nicola H. N. Yu, Hanry Chow, Vincent T. K. Chen, Jianzhu |
| author2 | Massachusetts Institute of Technology. Department of Biology |
| author_facet | Massachusetts Institute of Technology. Department of Biology Zheng, Dahai Limmon, Gino V. Yin, Lu Leung, Nicola H. N. Yu, Hanry Chow, Vincent T. K. Chen, Jianzhu |
| author_sort | Zheng, Dahai |
| collection | MIT |
| description | 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.. |
| first_indexed | 2024-09-23T13:26:31Z |
| format | Article |
| id | mit-1721.1/76658 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T13:26:31Z |
| publishDate | 2013 |
| publisher | Public Library of Science |
| record_format | dspace |
| spelling | mit-1721.1/766582022-09-28T14:15:12Z Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza Zheng, Dahai Limmon, Gino V. Yin, Lu Leung, Nicola H. N. Yu, Hanry Chow, Vincent T. K. Chen, Jianzhu Massachusetts Institute of Technology. Department of Biology Singapore-MIT Alliance in Research and Technology (SMART) Koch Institute for Integrative Cancer Research at MIT Chen, Jianzhu Zheng, Dahai Limmon, Gino V. Yin, Lu Leung, Nicola H. N. 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.. Singapore. National Research Foundation Singapore–MIT Alliance for Research and Technology (Infectious Disease-IRG research programme) 2013-01-30T16:37:12Z 2013-01-30T16:37:12Z 2012-10 2012-08 Article http://purl.org/eprint/type/JournalArticle 1932-6203 http://hdl.handle.net/1721.1/76658 Zheng, Dahai et al. “Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells Following Severe Pulmonary Damage Induced by Bleomycin and Influenza.” Ed. Saverio Bellusci. PLoS ONE 7.10 (2012): e48451. Web. https://orcid.org/0000-0002-5687-6154 en_US http://dx.doi.org/10.1371/journal.pone.0048451 PLoS One Creative Commons Attribution http://creativecommons.org/licenses/by/2.5/ application/pdf Public Library of Science PLoS |
| spellingShingle | Zheng, Dahai Limmon, Gino V. Yin, Lu Leung, Nicola H. N. Yu, Hanry Chow, Vincent T. K. Chen, Jianzhu Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza |
| title | Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza |
| title_full | Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza |
| title_fullStr | Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza |
| title_full_unstemmed | Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza |
| title_short | Regeneration of Alveolar Type I and II Cells from Scgb1a1-Expressing Cells following Severe Pulmonary Damage Induced by Bleomycin and Influenza |
| title_sort | regeneration of alveolar type i and ii cells from scgb1a1 expressing cells following severe pulmonary damage induced by bleomycin and influenza |
| url | http://hdl.handle.net/1721.1/76658 https://orcid.org/0000-0002-5687-6154 |
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