BACKGROUND: Damage to lung epithelial cells through chronic injury and abnormal repair and remodeling lead to lung destruction and fibrosis. We isolated lung progenitor cells that could potentially contribute to lung diseases. The progenitor cells can differentiate into alveolar type II (ATII)-like cells in vitro, and are increased in number and localized within the region of alveolar epithelial cell proliferation that is involved in the reparative response to injury. However, global gene expression patterns in the ATII-like cells derived from the progenitor cells and in mature ATII cells isolated from lung tissue have not yet been evaluated. METHODS: We performed gene expression array and directly compared the gene expression patterns in ATII-like cells derived from the progenitor cells with those in mature ATII cells isolated from human lung tissues. RESULTS: ATII-like cells and mature ATII cells expressed certain common genes, such as CEPBD and FOXP1, which determine the phenotypes of ATII cells. However, many genes were differentially expressed between the 2 cell types. As compared to mature ATII cells, ATII-like cells showed decreased expression of the genes associated with surfactant protein production and epithelial phenotypes. Pathway analysis indicated changes in several pathways, including those involved in epithelial-to-mesenchymal transition and receptor tyrosine kinase signaling, which could contribute to the observed differences in gene expression patterns. CONCLUSIONS: In this study, we identified genes commonly or differentially expressed by ATII-like cells differentiated from progenitor cells and mature ATII cells isolated from human lung tissues.
BACKGROUND: Damage to lung epithelial cells through chronic injury and abnormal repair and remodeling lead to lung destruction and fibrosis. We isolated lung progenitor cells that could potentially contribute to lung diseases. The progenitor cells can differentiate into alveolar type II (ATII)-like cells in vitro, and are increased in number and localized within the region of alveolar epithelial cell proliferation that is involved in the reparative response to injury. However, global gene expression patterns in the ATII-like cells derived from the progenitor cells and in mature ATII cells isolated from lung tissue have not yet been evaluated. METHODS: We performed gene expression array and directly compared the gene expression patterns in ATII-like cells derived from the progenitor cells with those in mature ATII cells isolated from human lung tissues. RESULTS: ATII-like cells and mature ATII cells expressed certain common genes, such as CEPBD and FOXP1, which determine the phenotypes of ATII cells. However, many genes were differentially expressed between the 2 cell types. As compared to mature ATII cells, ATII-like cells showed decreased expression of the genes associated with surfactant protein production and epithelial phenotypes. Pathway analysis indicated changes in several pathways, including those involved in epithelial-to-mesenchymal transition and receptor tyrosine kinase signaling, which could contribute to the observed differences in gene expression patterns. CONCLUSIONS: In this study, we identified genes commonly or differentially expressed by ATII-like cells differentiated from progenitor cells and mature ATII cells isolated from human lung tissues.
Authors: Daniel J Weiss; Daniel Chambers; Adam Giangreco; Armand Keating; Darrell Kotton; Peter I Lelkes; Darcy E Wagner; Darwin J Prockop Journal: Ann Am Thorac Soc Date: 2015-04