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PlGF mediates neutrophil elastase-induced airway epithelial cell apoptosis and emphysema

Overview of attention for article published in Respiratory Research, September 2014
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About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (60th percentile)
  • Above-average Attention Score compared to outputs of the same age and source (57th percentile)

Mentioned by

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5 tweeters

Citations

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16 Dimensions

Readers on

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23 Mendeley
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Title
PlGF mediates neutrophil elastase-induced airway epithelial cell apoptosis and emphysema
Published in
Respiratory Research, September 2014
DOI 10.1186/s12931-014-0106-1
Pubmed ID
Authors

Hsin-Han Hou, Shih-Lung Cheng, Kuei-Pin Chung, Shu-Chen Wei, Po-Nien Tsao, Hsuan-Hsuan Lu, Hao-Chien Wang, Chong-Jen Yu

Abstract

BackgroundChronic pulmonary obstructive disease (COPD) has become the fourth leading cause of death worldwide. Cigarette smoking induces neutrophil elastase (NE) and contributes to COPD, but the detailed mechanisms involved are not fully established. In an animal model of pulmonary emphysema, there are increased expressions of placenta growth factor (PlGF) and lung epithelial (LE) cell apoptosis. This study hypothesized that excessive NE may up-regulate PlGF and that PlGF-induced LE apoptosis mediates the pathogenesis of pulmonary emphysema.MethodsHuman bronchial epithelial cells, BEAS-2B, and primary mouse type II alveolar epithelial cells were treated with NE. The PlGF promoter activity was examined by luciferase activity assay, while PlGF expression and secretion were evaluated by RT-PCR, Western blotting, and ELISA. Both cell lines were treated with PlGF to evaluate its effects and the downstream signaling pathways leading to LE cell apoptosis. PlGF knockout and wild-type mice were instilled with NE to determine the roles of PlGF and its downstream molecules in NE-promoted mice pulmonary apoptosis and emphysema phenotype.ResultsThe transcriptional factor, early growth response gene-1, was involved in the NE-promoted PlGF promoter activity, and the expression and secretion of PlGF mRNA and protein in LE cells. PlGF-induced LE cell apoptosis and NE-induced mice pulmonary apoptosis and emphysema were mediated by the downstream c-Jun N-terminal kinase (JNK) and protein kinase C (PKC)¿ signaling pathways.ConclusionThe NE-PlGF-JNK/PKC¿ pathway contributes to the pathogenesis of LE cell apoptosis and emphysema. PlGF and its downstream signaling molecules may be potential therapeutic targets for COPD.

Twitter Demographics

The data shown below were collected from the profiles of 5 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 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 6 26%
Student > Bachelor 4 17%
Other 2 9%
Student > Master 2 9%
Unspecified 1 4%
Other 4 17%
Unknown 4 17%
Readers by discipline Count As %
Medicine and Dentistry 9 39%
Agricultural and Biological Sciences 5 22%
Biochemistry, Genetics and Molecular Biology 2 9%
Computer Science 1 4%
Unspecified 1 4%
Other 0 0%
Unknown 5 22%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 05 September 2014.
All research outputs
#6,794,631
of 12,537,999 outputs
Outputs from Respiratory Research
#773
of 1,467 outputs
Outputs of similar age
#76,425
of 201,400 outputs
Outputs of similar age from Respiratory Research
#10
of 28 outputs
Altmetric has tracked 12,537,999 research outputs across all sources so far. This one is in the 44th percentile – i.e., 44% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,467 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.0. This one is in the 41st percentile – i.e., 41% 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 201,400 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 60% of its contemporaries.
We're also able to compare this research output to 28 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 57% of its contemporaries.