| Circulating vascular progenitor cells do not contribute to compensatory lung growth. | |
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MedLine Citation:
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PMID: 12881479 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The biological principles that underlie the induction and process of alveolization in the lung as well as the maintenance of the complex lung tissue structure are one of the major obstacles in pulmonary medicine today. Bone marrow-derived cells have been shown to participate in angiogenesis, vascular repair, and remodeling of various organs. We addressed this phenomenon in the lung vasculature of mice in a model of regenerative lung growth. C57BL/6 mice were transplanted with bone marrow from one of three different reporter gene-transgenic strains. flk-1+/lacZ mice, tie-2/lacZ transgenic mice (both exhibiting endothelial cell-specific reporter gene expression), and ubiquitously enhanced green fluorescent protein (eGFP)-expressing mice served as marrow donors. After hematopoietic recovery, compensatory lung growth was induced by unilateral pneumonectomy and led to complete restoration of initial lung volume and surface area. The lungs were consecutively investigated for bone marrow-derived vascular cells by lacZ staining and immunohistochemistry for phenotype identification of vascular cells. lacZ- or eGFP-expressing bone marrow-derived endothelial cells could not be found in microvascular regions of alveolar septa. Single eGFP-positive endothelial cells were detected in pulmonary arteries at very low frequencies, whereas no eGFP-positive vascular smooth muscle cells were observed. In conclusion, we demonstrate in a model of lung growth and alveolization in adult mice the absence of significant bone marrow-derived progenitor cell contribution to the concomitant vascular growth and remodeling processes. |
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Authors:
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Robert Voswinckel; Tibor Ziegelhoeffer; Matthias Heil; Sawa Kostin; Georg Breier; Tanja Mehling; Rainer Haberberger; Matthias Clauss; Andreas Gaumann; Wolfgang Schaper; Werner Seeger |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2003-07-24 |
Journal Detail:
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Title: Circulation research Volume: 93 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2003 Aug |
Date Detail:
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Created Date: 2003-08-22 Completed Date: 2003-10-15 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 372-9 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University Clinic Giessen, Giessen, Germany. Robert.Voswinckel@innere.med.uni-giessen.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bone Marrow Cells / metabolism* Bone Marrow Transplantation* Endothelium, Vascular / metabolism Flow Cytometry Gene Expression Genotype Green Fluorescent Proteins Lac Operon / genetics Luminescent Proteins / genetics, metabolism Lung / growth & development*, metabolism Mice Mice, Inbred C57BL Mice, Transgenic Microscopy, Confocal Phenotype Pulmonary Alveoli / growth & development Receptor Protein-Tyrosine Kinases / genetics Receptor, TIE-2 Recombinant Fusion Proteins / genetics, metabolism Vascular Endothelial Growth Factor Receptor-2 / genetics |
| Chemical | |
Reg. No./Substance:
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0/Luminescent Proteins; 0/Recombinant Fusion Proteins; 147336-22-9/Green Fluorescent Proteins; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases; EC 2.7.10.1/Receptor, TIE-2; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-2 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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