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Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage
During late lung development, alveolar and microvascular development is finalized to enable sufficient gas exchange. Impaired late lung development manifests as bronchopulmonary dysplasia (BPD) in preterm infants. Single-cell RNA sequencing (scRNA-seq) allows for assessment of complex cellular dynam...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7946947/ https://www.ncbi.nlm.nih.gov/pubmed/33692365 http://dx.doi.org/10.1038/s41467-021-21865-2 |
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author | Hurskainen, Maria Mižíková, Ivana Cook, David P. Andersson, Noora Cyr-Depauw, Chanèle Lesage, Flore Helle, Emmi Renesme, Laurent Jankov, Robert P. Heikinheimo, Markku Vanderhyden, Barbara C. Thébaud, Bernard |
author_facet | Hurskainen, Maria Mižíková, Ivana Cook, David P. Andersson, Noora Cyr-Depauw, Chanèle Lesage, Flore Helle, Emmi Renesme, Laurent Jankov, Robert P. Heikinheimo, Markku Vanderhyden, Barbara C. Thébaud, Bernard |
author_sort | Hurskainen, Maria |
collection | PubMed |
description | During late lung development, alveolar and microvascular development is finalized to enable sufficient gas exchange. Impaired late lung development manifests as bronchopulmonary dysplasia (BPD) in preterm infants. Single-cell RNA sequencing (scRNA-seq) allows for assessment of complex cellular dynamics during biological processes, such as development. Here, we use MULTI-seq to generate scRNA-seq profiles of over 66,000 cells from 36 mice during normal or impaired lung development secondary to hyperoxia with validation of some of the findings in lungs from BPD patients. We observe dynamic populations of cells, including several rare cell types and putative progenitors. Hyperoxia exposure, which mimics the BPD phenotype, alters the composition of all cellular compartments, particularly alveolar epithelium, stromal fibroblasts, capillary endothelium and macrophage populations. Pathway analysis and predicted dynamic cellular crosstalk suggest inflammatory signaling as the main driver of hyperoxia-induced changes. Our data provides a single-cell view of cellular changes associated with late lung development in health and disease. |
format | Online Article Text |
id | pubmed-7946947 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-79469472021-03-28 Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage Hurskainen, Maria Mižíková, Ivana Cook, David P. Andersson, Noora Cyr-Depauw, Chanèle Lesage, Flore Helle, Emmi Renesme, Laurent Jankov, Robert P. Heikinheimo, Markku Vanderhyden, Barbara C. Thébaud, Bernard Nat Commun Article During late lung development, alveolar and microvascular development is finalized to enable sufficient gas exchange. Impaired late lung development manifests as bronchopulmonary dysplasia (BPD) in preterm infants. Single-cell RNA sequencing (scRNA-seq) allows for assessment of complex cellular dynamics during biological processes, such as development. Here, we use MULTI-seq to generate scRNA-seq profiles of over 66,000 cells from 36 mice during normal or impaired lung development secondary to hyperoxia with validation of some of the findings in lungs from BPD patients. We observe dynamic populations of cells, including several rare cell types and putative progenitors. Hyperoxia exposure, which mimics the BPD phenotype, alters the composition of all cellular compartments, particularly alveolar epithelium, stromal fibroblasts, capillary endothelium and macrophage populations. Pathway analysis and predicted dynamic cellular crosstalk suggest inflammatory signaling as the main driver of hyperoxia-induced changes. Our data provides a single-cell view of cellular changes associated with late lung development in health and disease. Nature Publishing Group UK 2021-03-10 /pmc/articles/PMC7946947/ /pubmed/33692365 http://dx.doi.org/10.1038/s41467-021-21865-2 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Hurskainen, Maria Mižíková, Ivana Cook, David P. Andersson, Noora Cyr-Depauw, Chanèle Lesage, Flore Helle, Emmi Renesme, Laurent Jankov, Robert P. Heikinheimo, Markku Vanderhyden, Barbara C. Thébaud, Bernard Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage |
title | Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage |
title_full | Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage |
title_fullStr | Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage |
title_full_unstemmed | Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage |
title_short | Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage |
title_sort | single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7946947/ https://www.ncbi.nlm.nih.gov/pubmed/33692365 http://dx.doi.org/10.1038/s41467-021-21865-2 |
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