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Increased S100A4 expression in the vasculature of human COPD lungs and murine model of smoke-induced emphysema

Overview of attention for article published in Respiratory Research, October 2015
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  • Above-average Attention Score compared to outputs of the same age (53rd percentile)
  • Average Attention Score compared to outputs of the same age and source

Mentioned by

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4 tweeters
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1 Google+ user

Citations

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28 Dimensions

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41 Mendeley
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Title
Increased S100A4 expression in the vasculature of human COPD lungs and murine model of smoke-induced emphysema
Published in
Respiratory Research, October 2015
DOI 10.1186/s12931-015-0284-5
Pubmed ID
Authors

Sebastian Reimann, Ludger Fink, Jochen Wilhelm, Julia Hoffmann, Mariola Bednorz, Michael Seimetz, Isabel Dessureault, Roger Troesser, Bahil Ghanim, Walter Klepetko, Werner Seeger, Norbert Weissmann, Grazyna Kwapiszewska

Abstract

Chronic obstructive lung disease (COPD) is a common cause of death in industrialized countries often induced by exposure to tobacco smoke. A substantial number of patients with COPD also suffer from pulmonary hypertension that may be caused by hypoxia or other hypoxia-independent stimuli - inducing pulmonary vascular remodeling. The Ca(2+) binding protein, S100A4 is known to play a role in non-COPD-driven vascular remodeling of intrapulmonary arteries. Therefore, we have investigated the potential involvement of S100A4 in COPD induced vascular remodeling. Lung tissue was obtained from explanted lungs of five COPD patients and five non-transplanted donor lungs. Additionally, mice lungs of a tobacco-smoke-induced lung emphysema model (exposure for 3 and 8 month) and controls were investigated. Real-time RT-PCR analysis of S100A4 and RAGE mRNA was performed from laser-microdissected intrapulmonary arteries. S100A4 immunohistochemistry was semi-quantitatively evaluated. Mobility shift assay and siRNA knock-down were used to prove hypoxia responsive elements (HRE) and HIF binding within the S100A4 promoter. Laser-microdissection in combination with real-time PCR analysis revealed higher expression of S100A4 mRNA in intrapulmonary arteries of COPD patients compared to donors. These findings were mirrored by semi-quantitative analysis of S100A4 immunostaining. Analogous to human lungs, in mice with tobacco-smoke-induced emphysema an up-regulation of S100A4 mRNA and protein was observed in intrapulmonary arteries. Putative HREs could be identified in the promoter region of the human S100A4 gene and their functionality was confirmed by mobility shift assay. Knock-down of HIF1/2 by siRNA attenuated hypoxia-dependent increase in S100A4 mRNA levels in human primary pulmonary artery smooth muscle cells. Interestingly, RAGE mRNA expression was enhanced in pulmonary arteries of tobacco-smoke exposed mice but not in pulmonary arteries of COPD patients. As enhanced S100A4 expression was observed in remodeled intrapulmonary arteries of COPD patients, targeting S100A4 could serve as potential therapeutic option for prevention of vascular remodeling in COPD patients.

Twitter Demographics

The data shown below were collected from the profiles of 4 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 41 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Canada 1 2%
Unknown 40 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 17%
Researcher 6 15%
Student > Master 6 15%
Student > Bachelor 3 7%
Professor 3 7%
Other 4 10%
Unknown 12 29%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 17%
Medicine and Dentistry 7 17%
Nursing and Health Professions 5 12%
Pharmacology, Toxicology and Pharmaceutical Science 2 5%
Agricultural and Biological Sciences 2 5%
Other 3 7%
Unknown 15 37%

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 21 October 2015.
All research outputs
#13,215,559
of 22,830,751 outputs
Outputs from Respiratory Research
#1,289
of 2,745 outputs
Outputs of similar age
#130,224
of 283,131 outputs
Outputs of similar age from Respiratory Research
#15
of 27 outputs
Altmetric has tracked 22,830,751 research outputs across all sources so far. This one is in the 41st percentile – i.e., 41% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,745 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.3. This one has gotten more attention than average, scoring higher than 50% 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 283,131 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 53% of its contemporaries.
We're also able to compare this research output to 27 others from the same source and published within six weeks on either side of this one. This one is in the 33rd percentile – i.e., 33% of its contemporaries scored the same or lower than it.