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Transforming growth factor beta1 targets estrogen receptor signaling in bronchial epithelial cells

Overview of attention for article published in Respiratory Research, August 2018
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Title
Transforming growth factor beta1 targets estrogen receptor signaling in bronchial epithelial cells
Published in
Respiratory Research, August 2018
DOI 10.1186/s12931-018-0861-5
Pubmed ID
Authors

L. Cody Smith, Santiago Moreno, Lauren Robertson, Sarah Robinson, Kristal Gant, Andrew J. Bryant, Tara Sabo-Attwood

Abstract

Sex differences in idiopathic pulmonary fibrosis (IPF) suggest a protective role for estrogen (E2); however, mechanistic studies in animal models have produced mixed results. Reports using cell lines have investigated molecular interactions between transforming growth factor beta1 (TGF-β1) and estrogen receptor (ESR) pathways in breast, prostate, and skin cells, but no such interactions have been described in human lung cells. To address this gap in the literature, we investigated a role for E2 in modulating TGF-β1-induced signaling mechanisms and identified novel pathways impacted by estrogen in bronchial epithelial cells. We investigated a role for E2 in modulating TGF-β1-induced epithelial to mesenchymal transition (EMT) in bronchial epithelial cells (BEAS-2Bs) and characterized the effect of TGF-β1 on ESR mRNA and protein expression in BEAS-2Bs. We also quantified mRNA expression of ESRs in lung tissue from individuals with IPF and identified potential downstream targets of E2 signaling in BEAS-2Bs using RNA-Seq and gene set enrichment analysis. E2 negligibly modulated TGF-β1-induced EMT; however, we report the novel observation that TGF-β1 repressed ESR expression, most notably estrogen receptor alpha (ESR1). Results of the RNA-Seq analysis showed that TGF-β1 and E2 inversely modulated the expression of several genes involved in processes such as extracellular matrix (ECM) turnover, airway smooth muscle cell contraction, and calcium flux regulation. We also report that E2 specifically modulated the expression of genes involved in chromatin remodeling pathways and that this regulation was absent in the presence of TGF-β1. Collectively, these results suggest that E2 influences unexplored pathways that may be relevant to pulmonary disease and highlights potential roles for E2 in the lung that may contribute to sex-specific differences.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 50 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 50 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 9 18%
Student > Bachelor 9 18%
Student > Master 7 14%
Student > Ph. D. Student 7 14%
Other 3 6%
Other 8 16%
Unknown 7 14%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 12 24%
Pharmacology, Toxicology and Pharmaceutical Science 7 14%
Agricultural and Biological Sciences 5 10%
Neuroscience 4 8%
Medicine and Dentistry 4 8%
Other 8 16%
Unknown 10 20%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 01 September 2018.
All research outputs
#14,920,631
of 25,385,509 outputs
Outputs from Respiratory Research
#1,499
of 3,062 outputs
Outputs of similar age
#176,518
of 344,376 outputs
Outputs of similar age from Respiratory Research
#35
of 66 outputs
Altmetric has tracked 25,385,509 research outputs across all sources so far. This one is in the 40th percentile – i.e., 40% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,062 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.9. This one is in the 48th percentile – i.e., 48% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 344,376 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 47th percentile – i.e., 47% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 66 others from the same source and published within six weeks on either side of this one. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.