Evidence map›Paper›PMID 23226399›Full record

ArticlePloS one2012

MiR-101 and miR-144 regulate the expression of the CFTR chloride channel in the lung.

Fatemat Hassan, Gerard J Nuovo, Melissa Crawford, Prosper N Boyaka, Stephen Kirkby, Serge P Nana-Sinkam, Estelle Cormet-Boyaka

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

89 citing papers in PubMed, 146 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. The Role of miR-144 in Inflammatory Diseases: A Review.Immunity, inflammation and disease · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Deletion of theAnnals of translational medicine · 2022
    Article
  20. Article

29 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Fatemat HassanDepartment of Internal Medicine, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, The Ohio State University, Columbus, OH, USA.
Gerard J Nuovo
Melissa Crawford
Prosper N Boyaka
Stephen Kirkby
Serge P Nana-Sinkam
Estelle Cormet-Boyaka
The Ohio State University · US

Funding

Toxic metals and ion channels in cigarette-smoke induced COPDR03HL095442 · NHLBI · OHIO STATE UNIVERSITY · PI CORMET-BOYAKA, ESTELLE A · 2009 to 2010
$150k
NHLBI NIH HHS R03 HL095442
6 · The paper itself

Abstract

The Cystic Fibrosis Transmembrane conductance Regulator (CFTR) is a chloride channel that plays a critical role in the lung by maintaining fluid homeostasis. Absence or malfunction of CFTR leads to Cystic Fibrosis, a disease characterized by chronic infection and inflammation. We recently reported that air pollutants such as cigarette smoke and cadmium negatively regulate the expression of CFTR by affecting several steps in the biogenesis of CFTR protein. MicroRNAs (miRNAs) have recently received a great deal of attention as both biomarkers and therapeutics due to their ability to regulate multiple genes. Here, we show that cigarette smoke and cadmium up-regulate the expression of two miRNAs (miR-101 and miR-144) that are predicted to target CFTR in human bronchial epithelial cells. When premature miR-101 and miR-144 were transfected in human airway epithelial cells, they directly targeted the CFTR 3'UTR and suppressed the expression of the CFTR protein. Since miR-101 was highly up-regulated by cigarette smoke in vitro, we investigated whether such increase also occurred in vivo. Mice exposed to cigarette smoke for 4 weeks demonstrated an up-regulation of miR-101 and suppression of CFTR protein in their lungs. Finally, we show that miR-101 is highly expressed in lung samples from patients with severe chronic obstructive pulmonary disease (COPD) when compared to control patients. Taken together, these results suggest that chronic cigarette smoking up-regulates miR-101 and that this miRNA could contribute to suppression of CFTR in the lungs of COPD patients.

Indexed as

Gene Expression Regulation3' Untranslated RegionsAir PollutantsAnimalsBase SequenceBronchiCadmiumCell LineCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsFemaleHumansLungMiceMice, Inbred C57BLMicroRNAs3' Untranslated RegionsAir PollutantsCadmiumCystic Fibrosis Transmembrane Conductance RegulatorMicroRNAsMIRN101 microRNA, humanMIRN101 microRNA, mouseMIRN144 microRNA, human

Identifiers

PMID23226399
PMCPMC3511328
OpenAlexW2017120774

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.