Austin E Gillen1, Rui Yang1, Calvin U Cotton2, Aura Perez2, Scott H Randell3, Shih-Hsing Leir4, Ann Harris5. 1. Human Molecular Genetics Program, Lurie Children's Research Center, Chicago, IL, 60614, United States; Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, United States. 2. Departments of Pediatrics, Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106, United States. 3. Marsico Lung Institute, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, United States. 4. Human Molecular Genetics Program, Lurie Children's Research Center, Chicago, IL, 60614, United States; Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, United States; Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44106, United States. 5. Human Molecular Genetics Program, Lurie Children's Research Center, Chicago, IL, 60614, United States; Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, United States; Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44106, United States. Electronic address: ann.harris@case.edu.
Abstract
BACKGROUND: Robust methods to culture primary airway epithelial cells were developed several decades ago and these cells provide the model of choice to investigate many diseases of the human lung. However, the molecular signature of cells from different regions of the airway epithelium has not been well characterized. METHODS: We utilize DNase-seq and RNA-seq to examine the molecular signatures of primary cells derived from human tracheal and bronchial tissues, as well as healthy and diseased (cystic fibrosis (CF)) donor lung tissue. RESULTS: Our data reveal an airway cell signature that is divergent from other epithelial cell types and from common airway epithelial cell lines. The differences between tracheal and bronchial cells are clearly evident as are common regulatory features. Only minor variation is seen between bronchial cells from healthy or CF donors. CONCLUSIONS: These data are a valuable resource for functional genomics analysis of airway epithelial tissues in human disease.
BACKGROUND: Robust methods to culture primary airway epithelial cells were developed several decades ago and these cells provide the model of choice to investigate many diseases of the human lung. However, the molecular signature of cells from different regions of the airway epithelium has not been well characterized. METHODS: We utilize DNase-seq and RNA-seq to examine the molecular signatures of primary cells derived from human tracheal and bronchial tissues, as well as healthy and diseased (cystic fibrosis (CF)) donor lung tissue. RESULTS: Our data reveal an airway cell signature that is divergent from other epithelial cell types and from common airway epithelial cell lines. The differences between tracheal and bronchial cells are clearly evident as are common regulatory features. Only minor variation is seen between bronchial cells from healthy or CF donors. CONCLUSIONS: These data are a valuable resource for functional genomics analysis of airway epithelial tissues in human disease.
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