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C-type natriuretic peptide ameliorates pulmonary fibrosis by acting on lung fibroblasts in mice

Overview of attention for article published in Respiratory Research, February 2016
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  • Good Attention Score compared to outputs of the same age (68th percentile)
  • Good Attention Score compared to outputs of the same age and source (72nd percentile)

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2 X users
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1 patent
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1 Facebook page

Citations

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Title
C-type natriuretic peptide ameliorates pulmonary fibrosis by acting on lung fibroblasts in mice
Published in
Respiratory Research, February 2016
DOI 10.1186/s12931-016-0335-6
Pubmed ID
Authors

Toru Kimura, Takashi Nojiri, Jun Hino, Hiroshi Hosoda, Koichi Miura, Yasushi Shintani, Masayoshi Inoue, Masahiro Zenitani, Hiroyuki Takabatake, Mikiya Miyazato, Meinoshin Okumura, Kenji Kangawa

Abstract

Pulmonary fibrosis has high rates of mortality and morbidity; however, no effective pharmacological therapy has been established. C-type natriuretic peptide (CNP), a member of the natriuretic peptide family, selectively binds to the transmembrane guanylyl cyclase (GC)-B receptor and exerts anti-inflammatory and anti-fibrotic effects in various organs through vascular endothelial cells and fibroblasts that have a cell-surface GC-B receptor. Given the pathophysiological importance of fibroblast activation in pulmonary fibrosis, we hypothesized that the anti-fibrotic and anti-inflammatory effects of exogenous CNP against bleomycin (BLM)-induced pulmonary fibrosis were exerted in part by the effect of CNP on pulmonary fibroblasts. C57BL/6 mice were divided into two groups, CNP-treated (2.5 μg/kg/min) and vehicle, to evaluate BLM-induced (1 mg/kg) pulmonary fibrosis and inflammation. A periostin-CNP transgenic mouse model exhibiting CNP overexpression in fibroblasts was generated and examined for the anti-inflammatory and anti-fibrotic effects of CNP via fibroblasts in vivo. Additionally, we assessed CNP attenuation of TGF-β-induced differentiation into myofibroblasts by using immortalized human lung fibroblasts stably expressing GC-B receptors. Furthermore, to investigate whether CNP acts on human lung fibroblasts in a clinical setting, we obtained primary-cultured fibroblasts from surgically resected lungs of patients with lung cancer and analyzed levels of GC-B mRNA transcription. CNP reduced mRNA levels of the profibrotic cytokines interleukin (IL)-1β and IL-6, as well as collagen deposition and the fibrotic area in lungs of mice with bleomycin-induced pulmonary fibrosis. Furthermore, similar CNP effects were observed in transgenic mice exhibiting fibroblast-specific CNP overexpression. In cultured-lung fibroblasts, CNP treatment attenuated TGF-β-induced phosphorylation of Smad2 and increased mRNA and protein expression of α-smooth muscle actin and SM22α, indicating that CNP suppresses fibroblast differentiation into myofibroblasts. Furthermore, human lung fibroblasts from patients with or without interstitial lung disease substantially expressed GC-B receptor mRNA. These data suggest that CNP ameliorates bleomycin-induced pulmonary fibrosis by suppressing TGF-β signaling and myofibroblastic differentiation in lung fibroblasts. Therefore, we propose consideration of CNP for clinical application to pulmonary fibrosis treatment.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 19%
Researcher 4 15%
Student > Doctoral Student 3 11%
Other 2 7%
Professor > Associate Professor 2 7%
Other 6 22%
Unknown 5 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 26%
Pharmacology, Toxicology and Pharmaceutical Science 3 11%
Agricultural and Biological Sciences 3 11%
Engineering 2 7%
Medicine and Dentistry 1 4%
Other 1 4%
Unknown 10 37%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 4. 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 10 March 2022.
All research outputs
#7,355,930
of 25,373,627 outputs
Outputs from Respiratory Research
#961
of 3,062 outputs
Outputs of similar age
#95,514
of 312,134 outputs
Outputs of similar age from Respiratory Research
#9
of 36 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one has received more attention than most of these and is in the 69th percentile.
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 has gotten more attention than average, scoring higher than 67% 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 312,134 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 68% of its contemporaries.
We're also able to compare this research output to 36 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 72% of its contemporaries.