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Caveolin-1 regulates the expression of tight junction proteins during hyperoxia-induced pulmonary epithelial barrier breakdown

Overview of attention for article published in Respiratory Research, May 2016
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Title
Caveolin-1 regulates the expression of tight junction proteins during hyperoxia-induced pulmonary epithelial barrier breakdown
Published in
Respiratory Research, May 2016
DOI 10.1186/s12931-016-0364-1
Pubmed ID
Authors

Shuyan Xu, Xindong Xue, Kai You, Jianhua Fu

Abstract

Bronchopulmonary dysplasia (BPD) is a common complication in preterm infants that involves the downregulation of tight junction (TJ) proteins. However, the mechanism underlying downregulation of the expression of TJ proteins during at the early stages of hyperoxia-induced BPD remains to be understood. Here, we aimed to identify the role of caveolin-1 (Cav-1) in hyperoxia-induced pulmonary epithelial barrier breakdown. First, we established an in vitro pulmonary epithelial barrier models using primary type II alveolar epithelial cells (AEC-II) from newborn rats. AEC-II was assigned to the hyperoxic (85 % O2/5 % CO2) or normoxic (21 % O2/5 % CO2) groups. Second, AEC-II was transfected with Cav-1-siRNA to downregulate Cav-1 under normoxic exposure. Third, AEC-II was transfected with a cDNA encoding Cav-1 to upregulate Cav-1 expression under hyperoxic exposure. Then, expression levels of Cav-1 and TJ proteins were examined by immunofluorescence staining, reverse transcription-polymerase chain reaction, and Western blotting. The TJ structures visualized using a transmission electron microscope, and transepithelial resistance and apparent permeability coefficient of fluorescein isothiocyanate-dextran, which are indicators of barrier function, were measured. Our data showed that exposure to hyperoxia disrupted the structure and function of the pulmonary epithelial barrier and decreased the ZO-1, occludin, claudin-4, and Cav-1 expression levels. Moreover, Cav-1 knockdown attenuated the expression of the other three genes and disrupted pulmonary epithelial barrier structure and function under normoxic exposure. However, Cav-1 upregulation markedly antagonized the hyperoxia-induced pulmonary epithelial barrier destruction and TJ protein loss. This is the first study to present evidence illustrating the novel role of Cav-1 downregulation-mediated TJ protein loss in pulmonary epithelial barrier destruction during BPD.

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The data shown below were collected from the profiles of 3 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 22%
Researcher 4 17%
Professor 2 9%
Student > Bachelor 2 9%
Other 1 4%
Other 2 9%
Unknown 7 30%
Readers by discipline Count As %
Immunology and Microbiology 4 17%
Biochemistry, Genetics and Molecular Biology 3 13%
Agricultural and Biological Sciences 3 13%
Medicine and Dentistry 2 9%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Other 1 4%
Unknown 9 39%
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 22 May 2016.
All research outputs
#14,913,921
of 25,373,627 outputs
Outputs from Respiratory Research
#1,499
of 3,062 outputs
Outputs of similar age
#164,179
of 326,216 outputs
Outputs of similar age from Respiratory Research
#21
of 43 outputs
Altmetric has tracked 25,373,627 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 326,216 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 48th percentile – i.e., 48% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 43 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.