Journal
SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-019-42819-1
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Funding
- National Institutes of Health (NIH) [5K12HD052896-09, 5T32HD007466-14]
- Hope Funds for Cancer Research [RO1 HL090136, R01 HL125821, R01 HL132266, U01 HL100402 RFA-HL-09-004]
- Basil O'Conner March of Dimes Starter Award
- Harvard Stem Cell Institute
- Pulmonary Fibrosis Foundation
- Boston Children's Hospital Office of Faculty Development
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Lung epithelial cell damage and dysfunctional repair play a role in the development of lung disease. Effective repair likely requires the normal functioning of alveolar stem/progenitor cells. For example, we have shown in a mouse model of bronchopulmonary dysplasia (BPD) that mesenchymal stem cells (MSC) protect against hyperoxic lung injury at least in part by increasing the number of Epcam(+) Sca-1(+) distal lung epithelial cells. These cells are capable of differentiating into both small airway (CCSP+) and alveolar (SPC+) epithelial cells in three-dimensional (3D) organoid cultures. To further understand the interactions between MSC and distal lung epithelial cells, we added MSC to lung progenitor 3D cultures. MSC stimulated Epcam(+) Sca-1(+ )derived organoid formation, increased alveolar differentiation and decreased self-renewal. MSC-conditioned media was sufficient to promote alveolar organoid formation, demonstrating that soluble factors secreted by MSC are likely responsible for the response. This work provides strong evidence of a direct effect of MSC-secreted factors on lung progenitor cell differentiation.
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