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The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury
BACKGROUND: Organ regeneration in mammals is hypothesized to require a functional pool of stem or progenitor cells, but the role of these cells in lung regeneration is unknown. METHODS: Based on the fact that postnatal regeneration of alveolar tissue has been attributed to alveolar epithelial cells,...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5141641/ https://www.ncbi.nlm.nih.gov/pubmed/27923370 http://dx.doi.org/10.1186/s12931-016-0480-y |
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author | Zeng, Ling Yang, Xue-tao Li, Hai-sheng Li, Yong Yang, Ce Gu, Wei Zhou, Yin-han Du, Juan Wang, Hai-yan Sun, Jian-hui Wen, Da-lin Jiang, Jian-xin |
author_facet | Zeng, Ling Yang, Xue-tao Li, Hai-sheng Li, Yong Yang, Ce Gu, Wei Zhou, Yin-han Du, Juan Wang, Hai-yan Sun, Jian-hui Wen, Da-lin Jiang, Jian-xin |
author_sort | Zeng, Ling |
collection | PubMed |
description | BACKGROUND: Organ regeneration in mammals is hypothesized to require a functional pool of stem or progenitor cells, but the role of these cells in lung regeneration is unknown. METHODS: Based on the fact that postnatal regeneration of alveolar tissue has been attributed to alveolar epithelial cells, we established a hemorrhagic shock and Lipopolysaccharide (LPS) lung injury model. Using this model, we analyzed the cellular kinetics of lung alveolar epithelial cells. RESULTS: The results showed that alveolar epithelium type 2 cells (AEC2s) are damage resistant during acute lung injury, they might be the main cells involved in lung injury and repair. Then we observed the relationship between the expression of HGF, c-Met following ALI in rat lung and proliferation of AEC2s. The proliferation of AEC2s was inhibited when isolated primary AEC2s were co-cultured with c-Met inhibitor SU11274. Furthermore, the numbers of AEC2s was significantly decreased when ALI rats were administrated with SU11274 in vivo. It provided further evidence that the HGF/c-Met signaling plays a vital role in ALI-induced AEC2s proliferation. CONCLUSIONS: AEC2s are damage resistant during acute lung injury and the HGF/c-Met signaling pathway is of vital importance in the proliferation of AEC2s after ALI. |
format | Online Article Text |
id | pubmed-5141641 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-51416412016-12-15 The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury Zeng, Ling Yang, Xue-tao Li, Hai-sheng Li, Yong Yang, Ce Gu, Wei Zhou, Yin-han Du, Juan Wang, Hai-yan Sun, Jian-hui Wen, Da-lin Jiang, Jian-xin Respir Res Research BACKGROUND: Organ regeneration in mammals is hypothesized to require a functional pool of stem or progenitor cells, but the role of these cells in lung regeneration is unknown. METHODS: Based on the fact that postnatal regeneration of alveolar tissue has been attributed to alveolar epithelial cells, we established a hemorrhagic shock and Lipopolysaccharide (LPS) lung injury model. Using this model, we analyzed the cellular kinetics of lung alveolar epithelial cells. RESULTS: The results showed that alveolar epithelium type 2 cells (AEC2s) are damage resistant during acute lung injury, they might be the main cells involved in lung injury and repair. Then we observed the relationship between the expression of HGF, c-Met following ALI in rat lung and proliferation of AEC2s. The proliferation of AEC2s was inhibited when isolated primary AEC2s were co-cultured with c-Met inhibitor SU11274. Furthermore, the numbers of AEC2s was significantly decreased when ALI rats were administrated with SU11274 in vivo. It provided further evidence that the HGF/c-Met signaling plays a vital role in ALI-induced AEC2s proliferation. CONCLUSIONS: AEC2s are damage resistant during acute lung injury and the HGF/c-Met signaling pathway is of vital importance in the proliferation of AEC2s after ALI. BioMed Central 2016-12-07 2016 /pmc/articles/PMC5141641/ /pubmed/27923370 http://dx.doi.org/10.1186/s12931-016-0480-y Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Zeng, Ling Yang, Xue-tao Li, Hai-sheng Li, Yong Yang, Ce Gu, Wei Zhou, Yin-han Du, Juan Wang, Hai-yan Sun, Jian-hui Wen, Da-lin Jiang, Jian-xin The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury |
title | The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury |
title_full | The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury |
title_fullStr | The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury |
title_full_unstemmed | The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury |
title_short | The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury |
title_sort | cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5141641/ https://www.ncbi.nlm.nih.gov/pubmed/27923370 http://dx.doi.org/10.1186/s12931-016-0480-y |
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