NDLI: Fibrocytes are not an essential source of type I collagen during lung fibrosis.

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Fibrocytes are not an essential source of type I collagen during lung fibrosis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Moore, Bethany B. Kleaveland, Kathryn R. Kim, Kevin K. Agarwal, Manisha Velikoff, Miranda Rippe, Richard A. Yang, Jibing
Description	Author Affiliation: Kleaveland KR ( Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109); Velikoff M ( Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109); Yang J ( Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109); Agarwal M ( Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109); Rippe RA ( National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892.); Moore BB ( Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109); Kim KK ( Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109)
Abstract	Progressive fibrosis involves accumulation of activated collagen-producing mesenchymal cells. Fibrocytes are hematopoietic-derived cells with mesenchymal features that potentially have a unique and critical function during fibrosis. Fibrocytes have been proposed as an important direct contributor of type I collagen deposition during fibrosis based largely on fate-mapping studies. To determine the functional contribution of hematopoietic cell-derived type I collagen to fibrogenesis, we use a double-transgenic system to specifically delete the type I collagen gene across a broad population of hematopoietic cells. These mice develop a robust fibrotic response similar to littermate genotype control mice injured with bleomycin indicating that fibrocytes are not a necessary source of type I collagen. Using collagen-promoter GFP mice, we find that fibrocytes express type I collagen. However, fibrocytes with confirmed deletion of the type I collagen gene have readily detectable intracellular type I collagen indicating that uptake of collagen from neighboring cells account for much of the fibrocyte collagen. Collectively, these results clarify several seemingly conflicting reports regarding the direct contribution of fibrocytes to collagen deposition.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400753
Journal	The Journal of Immunology
Issue Number	10
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-11-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Collagen Type I Deficiency Pulmonary Fibrosis Genetics Animals Bleomycin Cell Differentiation Cell Lineage Cells, Cultured Gene Expression Genes, Reporter Green Fluorescent Proteins Metabolism Mice Mice, Transgenic Promoter Regions, Genetic Protein Transport Chemically Induced Pathology Stromal Cells Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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