↓ Skip to main content

Combination of glycopyrronium and indacaterol inhibits carbachol-induced ERK5 signal in fibrotic processes

Overview of attention for article published in Respiratory Research, March 2017
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age

Mentioned by

twitter
4 X users

Citations

dimensions_citation
5 Dimensions

Readers on

mendeley
16 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Combination of glycopyrronium and indacaterol inhibits carbachol-induced ERK5 signal in fibrotic processes
Published in
Respiratory Research, March 2017
DOI 10.1186/s12931-017-0529-6
Pubmed ID
Authors

Yukiko Namba, Shinsaku Togo, Miniwan Tulafu, Kotaro Kadoya, Kumi Yoneda Nagahama, Hikari Taka, Naoko Kaga, Akira Orimo, Xiangde Liu, Kazuhisa Takahashi

Abstract

Airway fibrosis is one of the pathological features of chronic obstructive pulmonary disease (COPD), and recent studies revealed that acetylcholine plays an important role in the development of airway remodeling by stimulating proliferation and collagen synthesis of lung fibroblasts. This study was designed to examine the effects of a long-acting muscarinic receptor antagonist (LAMA) glycopyrronium and a long-acting β2 adrenergic receptor agonist (LABA) indacaterol on acetylcholine-mediated fibrotic responses in lung fibroblasts. After carbachol (CCh) or transforming growth factor-β1 (TGF-β1) exposure, the response to glycopyrronium and indacaterol was determined in vitro in fibroblasts isolated from mild-to-moderate COPD lung tissue. The ability of fibroblasts to mediate the contraction of collagen gels was assessed. The expression of α-smooth muscle actin (α-SMA) and the phosphorylation of extracellular-signal-regulated kinase 5 (ERK5) were determined by immunoblot. TGF-β1 was quantified by ELISA and acetylcholine was quantified by liquid chromatography tandem-mass spectrometry. CCh stimulated fibroblast-mediated collagen gel contraction and α-SMA expression and TGF-β1 release by fibroblasts. Blockade of autocrine TGF-β1 attenuated CCh-mediated fibrotic responses, while TGF-β1 did not stimulate acetylcholine release. Glycopyrronium plus indacaterol significantly attenuated CCh- and TGF-β1-mediated fibrotic responses through inhibition of ERK5 phosphorylation. Notably, the magnitudes of CCh- and TGF-β1-stimulated gel contraction, CCh-induced TGF-β1 release, and ERK5 phosphorylation were greater in fibroblasts isolated from COPD subjects than in those from non-smokers. CCh induced TGF-β1 self-sustaining signaling loops by potentiating ERK5 signaling and promoted myofibroblast activity. This autocrine signaling mechanism may be an attractive therapeutic target to block the fibrotic response, which was modulated by the combination of glycopyrronium and indacaterol.

X Demographics

X Demographics

The data shown below were collected from the profiles of 4 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 16 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 16 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 3 19%
Other 2 13%
Student > Doctoral Student 1 6%
Unspecified 1 6%
Student > Master 1 6%
Other 3 19%
Unknown 5 31%
Readers by discipline Count As %
Medicine and Dentistry 3 19%
Agricultural and Biological Sciences 2 13%
Business, Management and Accounting 1 6%
Unspecified 1 6%
Social Sciences 1 6%
Other 1 6%
Unknown 7 44%
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 02 December 2017.
All research outputs
#16,725,651
of 25,382,440 outputs
Outputs from Respiratory Research
#2,055
of 3,062 outputs
Outputs of similar age
#197,008
of 321,626 outputs
Outputs of similar age from Respiratory Research
#36
of 47 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% 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 27th percentile – i.e., 27% 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 321,626 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 35th percentile – i.e., 35% 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 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.