Evidence map›Paper›PMID 27060571›Full record

ArticleFEBS letters2016

Airway smooth muscle inflammation is regulated by microRNA-145 in COPD.

Lawrence O'Leary, Kenan Sevinç, Ilektra M Papazoglou, Bernadett Tildy, Karen Detillieux, Andrew J Halayko, Kian Fan Chung, Mark M Perry

Open access · hybridAbstract readLetter
In one paragraph

Article in FEBS letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
9.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Plasma miR-150-5p as a Biomarker for Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. COPD-associated miR-145-5p is downregulated in early-decline FEVThe Journal of allergy and clinical immunology · 2021
    Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 4 countries.

Lawrence O'LearyAirways Disease, National Heart and Lung Institute, Imperial College, London, UK.
Kenan SevinçAirways Disease, National Heart and Lung Institute, Imperial College, London, UK.
Ilektra M PapazoglouAirways Disease, National Heart and Lung Institute, Imperial College, London, UK.
Bernadett TildyAirways Disease, National Heart and Lung Institute, Imperial College, London, UK.
Karen DetillieuxDepartments of Internal Medicine & Physiology, Respiratory Hospital, Winnipeg, MB, Canada.
Andrew J HalaykoDepartments of Internal Medicine & Physiology, Respiratory Hospital, Winnipeg, MB, Canada.
Kian Fan ChungAirways Disease, National Heart and Lung Institute, Imperial College, London, UK.
Mark M PerryMolecular Neurosciences, The Dubowitz Neuromuscular Centre, UCL Institute of Child Health, London, UK.ORCID 0000-0002-8145-8042
Lung Institute · USManitoba Beekeepers' Association · CAInstitute of Child Health · IN

Funding

Department of HealthWellcome Trust 085935
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease, in part caused by the aberrant function of airway smooth muscle (ASM) cells under the regulation of transforming growth factor (TGF)-β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA-145 (miR-145) may interact with SMAD3, an important downstream signalling molecule of the TGF-β pathway. TGF-β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF-β-dependent increase in CXCL8 and IL-6 release, most notably in the cells from COPD patients. TGF-β stimulation increased SMAD3 expression, only in cells from COPD patients, with a concurrent increased miR-145 expression. Regulation of miR-145 was found to be negatively controlled by pathways involving the MAP kinases, MEK-1/2 and p38 MAPK. Subsequent, overexpression of miR-145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL-6 and CXCL8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR-145 negatively regulates pro-inflammatory cytokine release from ASM cells in COPD by targeting SMAD3.

Indexed as

AgedCase-Control StudiesCells, CulturedFemaleHumansInflammationInterleukin-6Interleukin-8LungMaleMAP Kinase Signaling SystemMicroRNAsMiddle AgedMuscle, SmoothPulmonary Disease, Chronic ObstructiveSmad3 ProteinInterleukin-6Interleukin-8MicroRNAsMIRN145 microRNA, humanSmad3 ProteinSMAD3 protein, humanCOPDinflammationmicroRNA

Identifiers

PMID27060571
PMCPMC5082497
OpenAlexW2329713786

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.