10.5061/DRYAD.31NB080
Tovar, Adelaide
University of North Carolina at Chapel Hill
Smith, Gregory J.
University of North Carolina at Chapel Hill
Thomas, Joseph M.
University of North Carolina at Chapel Hill
Crouse, Wesley L.
0000-0001-5745-4490
University of North Carolina at Chapel Hill
Harkema, Jack R.
Michigan State University
Kelada, Samir N. P.
0000-0003-2676-9232
University of North Carolina at Chapel Hill
Data from: Transcriptional profiling of the murine airway response to
acute ozone exposure
Dryad
dataset
2019
lung
mouse
injury
2019-10-19T00:00:00Z
2019-10-19T00:00:00Z
en
35420488 bytes
5
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Ambient ozone (O3) exposure has serious consequences on respiratory
health, including airway inflammation and injury. Decades of research have
yielded thorough descriptions of these outcomes; however, less is known
about the molecular processes that drive them. The aim of this study was
to further describe the cellular and molecular responses to O3 exposure in
murine airways, with a particular focus on transcriptional responses in
two critical compartments: conducting airways (CA) and airway macrophages
(AM). After exposing adult, female C57BL/6J mice to filtered air, 1 or 2
ppm O3, we assessed hallmark responses including airway inflammation (cell
counts and cytokine secretion) and injury (epithelial permeability),
followed by gene expression profiling of CA and AM by RNA-seq. As
expected, we observed concentration-dependent increases in airway
inflammation and injury. CA and AM both exhibited changes in gene
expression to both 1 and 2 ppm O3 that were largely compartment-specific.
In CA, genes associated with epithelial barrier function, detoxification
processes, and cellular proliferation were altered, while O3 affected
genes involved in innate immune signaling, cytokine production, and
extracellular matrix remodeling in AM. Further, CA and AM also exhibited
notable differences in concentration-response expression patterns for
large numbers of genes. Overall, our study has described transcriptional
responses to acute O3 exposure, revealing both shared and unique gene
expression patterns across multiple concentrations of O3 and in two
important O3-responsive tissues. These profiles provide broad mechanistic
insight into pulmonary O3 toxicity, and reveal a variety of targets for
focused follow-up studies.
Phenotyping dataraw phenotyping data.csvOrdered-factor model analysis and
dataOrdered-factor model analysis including input data files and
codeOrdered factor model analysis and data.zipR files for
figures/analysisR files for generating manuscript figures and gene
expression analysesManuscript figures and gene expression
analysis.zipSupplementary DataSupplementary data files including all
output from DESeq2 gene expression analysis and GSVASupplementary
TablesSupplementary tables referenced in the textSupplementary Figure
1Supplementary figure 1 referenced in the text (CA marker genes)supp
fig1.tifSupplementary Figure 2Supplementary figure 2 referenced in the
text (AM polarization genes)supp fig2.tifManuscript figures and gene
expression analysisR code files to generate figures and gene expression
analyses