NDLI: Epithelial ß1 integrin is required for lung branching morphogenesis and alveolarization.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Plosa, Erin J. Young, Lisa R. Gulleman, Peter M. Polosukhin, Vasiliy V. Zaynagetdinov, Rinat Benjamin, John T. Im, Amanda M. Van Der Meer, Riet Gleaves, Linda A. Bulus, Nada Han, Wei Prince, Lawrence S. Blackwell, Timothy S. Zent, Roy
Description	Country affiliation: United States Author Affiliation: Plosa EJ ( Department of Pediatrics, Division of Neonatology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Young LR ( Department of Pediatrics, Division of Pulmonary Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA Department of Cell and Developme); Gulleman PM ( Department of Pediatrics, Division of Pulmonary Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Polosukhin VV ( Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Zaynagetdinov R ( Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Benjamin JT ( Department of Pediatrics, Division of Neonatology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Im AM ( Department of Pediatrics, Division of Neonatology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); van der Meer R ( Department of Pediatrics, Division of Neonatology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Gleaves LA ( Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Bulus N ( Department of Medicine, Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Han W ( Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.); Prince LS ( Department of Pediatrics, Division of Neonatology, University of California San Diego, San Diego, CA 92103, USA.); Blackwell TS ( Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA Department of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, TN 37232, USA Department of Cancer Biology, Vanderbilt Uni); Zent R ( Department of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, TN 37232, USA Department of Medicine, Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN 37232, USA Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, T)
Abstract	Integrin-dependent interactions between cells and extracellular matrix regulate lung development; however, specific roles for ß1-containing integrins in individual cell types, including epithelial cells, remain incompletely understood. In this study, the functional importance of ß1 integrin in lung epithelium during mouse lung development was investigated by deleting the integrin from E10.5 onwards using surfactant protein C promoter-driven Cre. These mutant mice appeared normal at birth but failed to gain weight appropriately and died by 4âmonths of age with severe hypoxemia. Defects in airway branching morphogenesis in association with impaired epithelial cell adhesion and migration, as well as alveolarization defects and persistent macrophage-mediated inflammation were identified. Using an inducible system to delete ß1 integrin after completion of airway branching, we showed that alveolarization defects, characterized by disrupted secondary septation, abnormal alveolar epithelial cell differentiation, excessive collagen I and elastin deposition, and hypercellularity of the mesenchyme occurred independently of airway branching defects. By depleting macrophages using liposomal clodronate, we found that alveolarization defects were secondary to persistent alveolar inflammation. ß1 integrin-deficient alveolar epithelial cells produced excessive monocyte chemoattractant protein 1 and reactive oxygen species, suggesting a direct role for ß1 integrin in regulating alveolar homeostasis. Taken together, these studies define distinct functions of epithelial ß1 integrin during both early and late lung development that affect airway branching morphogenesis, epithelial cell differentiation, alveolar septation and regulation of alveolar homeostasis.
File Format	HTM / HTML
ISSN	09501991
e-ISSN	14779129
DOI	10.1242/dev.117200
Journal	Development
Issue Number	24
Volume Number	141
Language	English
Publisher	The Company of Biologists
Publisher Date	2014-12-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Developmental Discipline Biology Antigens, Cd29 Metabolism Epithelial Cells Lung Embryology Organogenesis Physiology Pulmonary Alveoli Animals Bronchoalveolar Lavage Cell Adhesion Cell Movement Chemokine Ccl2 Enzyme-linked Immunosorbent Assay Extracellular Matrix Integrases Mice Microscopy, Confocal Pulmonary Surfactant-associated Protein C Reactive Oxygen Species Thiobarbituric Acid Reactive Substances Research Support, N.i.h., Extramural Research Support, U.s. Gov't, Non-p.h.s.
Content Type	Text
Resource Type	Article
Subject	Developmental Biology Molecular Biology

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