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MicroRNA-181c inhibits cigarette smoke–induced chronic obstructive pulmonary disease by regulating CCN1 expression

Overview of attention for article published in Respiratory Research, August 2017
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Title
MicroRNA-181c inhibits cigarette smoke–induced chronic obstructive pulmonary disease by regulating CCN1 expression
Published in
Respiratory Research, August 2017
DOI 10.1186/s12931-017-0639-1
Pubmed ID
Authors

Yong Du, Yi Ding, Xuru Chen, Zhoufang Mei, Heyuan Ding, Yi Wu, Zhijun Jie

Abstract

Chronic obstructive pulmonary disease (COPD) is an obstinate pulmonary disease, causing irreversible alveoli collapse and increasing the risk for cardiovascular disease. Accumulating evidence has shown that the dysregulation of miRNAs is crucially involved in the pathogenesis and development of COPD. However, the effects and role of microRNA-181c (miR-181c) have not been investigated in a murine model of COPD. miR-181c expression was detected in human lung tissue samples of 34 patients, an in vivo murine model of CS exposure, and primary human bronchial epithelial cells (HBECs) by qRT-PCR. Degeneration of lung tissue, necrosis, infiltration and neutrophil cells were assessed with H&E and flow cytometry. Interleukin (IL)-6 and IL-8 levels were determined by an enzyme-linked immunosorbent assay and qRT-PCR. Luciferase reporter assay and correlation analyses were used to confirm and measure the levels between miR-181c and its target CCN1. We showed that miR-181c was significantly down-regulated in lung tissues from patients with COPD compared to individuals who had never smoked (p < 0.01). We also observed a down-regulation of miR-181c in HBECs and a mouse model after cigarette smoke (CS) exposure. Functional assays demonstrated that miR-181c over-expression decreased the inflammatory response, neutrophil infiltration, reactive oxygen species (ROS) generation, and inflammatory cytokines induced by CS, while its down-regulation produced the opposite effects. Subsequent investigation found that CCN1 was a direct target of miR-181c. CCN1 expression was increased in lung tissues of COPD patients, and was negatively correlated with miR-181c expression in human COPD samples (p < 0.01). Taken together, our data suggest the critical roles of miR-181c and its target CCN1 in COPD development, and provide potential therapeutic targets for COPD treatment.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 50 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 50 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 12 24%
Student > Bachelor 7 14%
Student > Ph. D. Student 5 10%
Student > Doctoral Student 3 6%
Student > Master 3 6%
Other 3 6%
Unknown 17 34%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 14%
Medicine and Dentistry 6 12%
Pharmacology, Toxicology and Pharmaceutical Science 3 6%
Nursing and Health Professions 3 6%
Agricultural and Biological Sciences 3 6%
Other 9 18%
Unknown 19 38%
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 08 May 2018.
All research outputs
#15,173,117
of 25,382,440 outputs
Outputs from Respiratory Research
#1,601
of 3,062 outputs
Outputs of similar age
#169,388
of 326,133 outputs
Outputs of similar age from Respiratory Research
#30
of 43 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 38th percentile – i.e., 38% 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 43rd percentile – i.e., 43% 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 326,133 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 43 others from the same source and published within six weeks on either side of this one. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.