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Role of Matrix Metalloproteinases-1 and -2 in Interleukin-13–Suppressed Elastin in Airway Fibroblasts in Asthma

Overview of attention for article published in American Journal of Respiratory Cell and Molecular Biology, January 2016
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Title
Role of Matrix Metalloproteinases-1 and -2 in Interleukin-13–Suppressed Elastin in Airway Fibroblasts in Asthma
Published in
American Journal of Respiratory Cell and Molecular Biology, January 2016
DOI 10.1165/rcmb.2014-0290oc
Pubmed ID
Authors

Jennifer L. Ingram, David Slade, Tony D. Church, Dave Francisco, Karissa Heck, R. Wesley Sigmon, Michael Ghio, Anays Murillo, Rafael Firszt, Njira L. Lugogo, Loretta Que, Mary E. Sunday, Monica Kraft

Abstract

Elastin synthesis and degradation in the airway and lung parenchyma contribute to airway mechanics, including airway patency and elastic recoil. Interleukin (IL)-13 mediates many features of asthma pathobiology, including airway remodeling, but the effects of IL-13 on elastin architecture in the airway wall are not known. We hypothesized that IL-13 modulates elastin expression in airway fibroblasts from subjects with allergic asthma. 25 subjects with mild asthma (FEV1: 89 ± 3% pred) and 30 normal controls (FEV1: 102 ± 2% pred) underwent bronchoscopy with endobronchial biopsy. Elastic fibers were visualized in airway biopsy specimens using Weigert's resorcin-fuchsin elastic stain. Airway fibroblasts were exposed to IL-13, a pan-matrix metalloproteinase (MMP) inhibitor (GM6001), specific inhibitors to MMP-1, -2, -3 and -8, and combinations of IL-13 with MMP inhibitors in separate conditions in serum-free media for 48 hours. Elastin (ELN) expression as well as MMP secretion and activity were quantified. Elastic fiber staining of airway biopsy tissue was significantly associated with methacholine PC20 levels in asthma patients. IL-13 significantly suppressed ELN expression in asthmatic airway fibroblasts as compared to normal controls. The effect of IL-13 on ELN expression was significantly correlated with post-bronchodilator FEV1/FVC in asthmatic patients. MMP inhibition significantly stimulated ELN expression in asthma as compared to normal controls. Specific inhibition of MMP-1 and MMP-2, but not MMP-3 or MMP-8, reversed the IL-13-induced suppression of ELN expression. In asthma, MMP-1 and MMP-2 mediate IL-13-induced suppression of ELN expression in airway fibroblasts.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 4%
Unknown 25 96%

Demographic breakdown

Readers by professional status Count As %
Other 4 15%
Student > Master 4 15%
Researcher 3 12%
Student > Ph. D. Student 3 12%
Professor > Associate Professor 2 8%
Other 3 12%
Unknown 7 27%
Readers by discipline Count As %
Medicine and Dentistry 8 31%
Biochemistry, Genetics and Molecular Biology 3 12%
Engineering 2 8%
Immunology and Microbiology 2 8%
Business, Management and Accounting 1 4%
Other 3 12%
Unknown 7 27%
Attention Score in Context

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 03 May 2016.
All research outputs
#14,229,946
of 22,813,792 outputs
Outputs from American Journal of Respiratory Cell and Molecular Biology
#2,372
of 3,350 outputs
Outputs of similar age
#205,929
of 393,465 outputs
Outputs of similar age from American Journal of Respiratory Cell and Molecular Biology
#29
of 47 outputs
Altmetric has tracked 22,813,792 research outputs across all sources so far. This one is in the 35th percentile – i.e., 35% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,350 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.1. This one is in the 25th percentile – i.e., 25% 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 393,465 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 47 others from the same source and published within six weeks on either side of this one. This one is in the 31st percentile – i.e., 31% of its contemporaries scored the same or lower than it.