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论文题目: Contribution of Fetal, but Not Adult, Pulmonary Mesothelium to Mesenchymal Lineages in Lung Homeostasis and Fibrosis
英文论文题目: Contribution of Fetal, but Not Adult, Pulmonary Mesothelium to Mesenchymal Lineages in Lung Homeostasis and Fibrosis
第一作者: von Gise, A; Stevens, SM; Honor, LB; Oh, JH; Gao, C; Zhou, B; Pu, WT
英文第一作者: von Gise, A; Stevens, SM; Honor, LB; Oh, JH; Gao, C; Zhou, B; Pu, WT
联系作者: Pu, WT (reprint author), Catholic Univ Korea, Dept Pediat, Seoul, South Korea.
英文联系作者: Pu, WT (reprint author), Catholic Univ Korea, Dept Pediat, Seoul, South Korea.
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发表年度: 2016
卷: 54
期: 2
页码: 222-230
摘要: The lung is enveloped by a layer of specialized epithelium, the pulmonary mesothelium. In other organs, mesothelial cells undergo epithelialmesenchymal transition and contribute to organ stromal cells. The contribution of pulmonary mesothelial cells (PMCs) to the developing lung has been evaluated with differing conclusions. PMCs have also been indirectly implicated in lung fibrosis in the progressive, fatal lung disease idiopathic pulmonary fibrosis. We used fetal or postnatal genetic pulse labeling of PMCs to assess their fate in murine development, normal lung homeostasis, and models of pulmonary fibrosis. We found that most fetal PMC-derived mesenchymal cells (PMCDCs) expressed markers of pericytes and fibroblasts, only a small minority expressed smooth muscle markers, and none expressed endothelial cell markers. Postnatal PMCs did not contribute to lung mesenchyme during normal lung homeostasis or in models of lung fibrosis. However, fetal PMCDCs were abundant and actively proliferating within fibrotic regions in lung fibrosis models, suggesting that they actively participate in the fibrotic process. These data clarify the role of fetal and postnatal PMCDCs in lung development and disease.
英文摘要: The lung is enveloped by a layer of specialized epithelium, the pulmonary mesothelium. In other organs, mesothelial cells undergo epithelialmesenchymal transition and contribute to organ stromal cells. The contribution of pulmonary mesothelial cells (PMCs) to the developing lung has been evaluated with differing conclusions. PMCs have also been indirectly implicated in lung fibrosis in the progressive, fatal lung disease idiopathic pulmonary fibrosis. We used fetal or postnatal genetic pulse labeling of PMCs to assess their fate in murine development, normal lung homeostasis, and models of pulmonary fibrosis. We found that most fetal PMC-derived mesenchymal cells (PMCDCs) expressed markers of pericytes and fibroblasts, only a small minority expressed smooth muscle markers, and none expressed endothelial cell markers. Postnatal PMCs did not contribute to lung mesenchyme during normal lung homeostasis or in models of lung fibrosis. However, fetal PMCDCs were abundant and actively proliferating within fibrotic regions in lung fibrosis models, suggesting that they actively participate in the fibrotic process. These data clarify the role of fetal and postnatal PMCDCs in lung development and disease.
刊物名称: AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
英文刊物名称: AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
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学科: Biochemistry & Molecular Biology; Cell Biology; Respiratory System
英文学科: Biochemistry & Molecular Biology; Cell Biology; Respiratory System
影响因子: 4.1
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论文类别: Article
英文论文类别: Article
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