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Tight junction disruption by cadmium in an in vitro human airway tissue model

Overview of attention for article published in Respiratory Research, February 2015
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (90th percentile)

Mentioned by

news
2 news outlets
twitter
2 tweeters
facebook
1 Facebook page
googleplus
1 Google+ user

Citations

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49 Dimensions

Readers on

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57 Mendeley
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Title
Tight junction disruption by cadmium in an in vitro human airway tissue model
Published in
Respiratory Research, February 2015
DOI 10.1186/s12931-015-0191-9
Pubmed ID
Authors

Xuefei Cao, Haixia Lin, Levan Muskhelishvili, John Latendresse, Patricia Richter, Robert H Heflich

Abstract

The cadmium (Cd) present in air pollutants and cigarette smoke has the potential of causing multiple adverse health outcomes involving damage to pulmonary and cardiovascular tissue. Injury to pulmonary epithelium may include alterations in tight junction (TJ) integrity, resulting in impaired epithelial barrier function and enhanced penetration of chemicals and biomolecules. Herein, we investigated mechanisms involved in the disruption of TJ integrity by Cd exposure using an in vitro human air-liquid-interface (ALI) airway tissue model derived from normal primary human bronchial epithelial cells. ALI cultures were exposed to noncytotoxic doses of CdCl2 basolaterally and TJ integrity was measured by Trans-Epithelial Electrical Resistance (TEER) and immunofluorescence staining with TJ markers. PCR array analysis was used to identify genes involved with TJ collapse. To explore the involvement of kinase signaling pathways, cultures were treated with CdCl2 in the presence of kinase inhibitors specific for cellular Src or Protein Kinase C (PKC). Noncytotoxic doses of CdCl2 resulted in the collapse of barrier function, as demonstrated by TEER measurements and Zonula occludens-1 (ZO-1) and occludin staining. CdCl2 exposure altered the expression of several groups of genes encoding proteins involved in TJ homeostasis. In particular, down-regulation of select junction-interacting proteins suggested that a possible mechanism for Cd toxicity involves disruption of the peripheral junctional complexes implicated in connecting membrane-bound TJ components to the actin cytoskeleton. Inhibition of kinase signaling using inhibitors specific for cellular Src or PKC preserved the integrity of TJs, possibly by preventing occludin tyrosine hyperphosphorylation, rather than reversing the down-regulation of the junction-interacting proteins. Our findings indicate that acute doses of Cd likely disrupt TJ integrity in human ALI airway cultures both through occludin hyperphosphorylation via kinase activation and by direct disruption of the junction-interacting complex.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 57 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 2%
France 1 2%
Unknown 55 96%

Demographic breakdown

Readers by professional status Count As %
Researcher 12 21%
Other 9 16%
Student > Ph. D. Student 8 14%
Student > Bachelor 5 9%
Student > Doctoral Student 5 9%
Other 10 18%
Unknown 8 14%
Readers by discipline Count As %
Agricultural and Biological Sciences 13 23%
Medicine and Dentistry 8 14%
Pharmacology, Toxicology and Pharmaceutical Science 6 11%
Biochemistry, Genetics and Molecular Biology 4 7%
Environmental Science 4 7%
Other 10 18%
Unknown 12 21%

Attention Score in Context

This research output has an Altmetric Attention Score of 18. 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 28 December 2020.
All research outputs
#1,437,541
of 19,846,165 outputs
Outputs from Respiratory Research
#110
of 2,420 outputs
Outputs of similar age
#20,381
of 227,570 outputs
Outputs of similar age from Respiratory Research
#1
of 1 outputs
Altmetric has tracked 19,846,165 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 92nd percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,420 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.0. This one has done particularly well, scoring higher than 95% of its peers.
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 227,570 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 90% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them