Evidence map›Paper›PMID 30595527›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2019

A Neutralizing Aptamer to TGFBR2 and miR-145 Antagonism Rescue Cigarette Smoke- and TGF-β-Mediated CFTR Expression.

Rajib K Dutta, Srinivasan Chinnapaiyan, Lawrence Rasmussen, S Vamsee Raju, Hoshang J Unwalla

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

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  16. Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022
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  18. Article
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  20. The Multifaceted Roles of MicroRNAs in Cystic Fibrosis.Diagnostics (Basel, Switzerland) · 2020
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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

5 authors at 2 institutions in 1 country.

Rajib K DuttaDepartment of Immunology and Nanomedicine, Institute of Neuroimmune Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.
Srinivasan ChinnapaiyanDepartment of Immunology and Nanomedicine, Institute of Neuroimmune Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.
Lawrence RasmussenDivision of Pulmonary, Allergy, and Critical Care Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
S Vamsee RajuDivision of Pulmonary, Allergy, and Critical Care Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Hoshang J UnwallaDepartment of Immunology and Nanomedicine, Institute of Neuroimmune Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA. Electronic address: hunwalla@fiu.edu.
Florida International University · USUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor β (TGF-β), signaling induced by cigarette smoke (CS), plays an important role in the progression of airway diseases, like chronic bronchitis associated with chronic obstructive pulmonary disease (COPD), and in smokers. Chronic bronchitis is characterized by reduced mucociliary clearance (MCC). Cystic fibrosis transmembrane conductance regulator (CFTR) plays an important role in normal MCC. TGF-β and CS (via TGF-β) promote acquired CFTR dysfunction by suppressing CFTR biogenesis and function. Understanding the mechanism by which CS promotes CFTR dysfunction can identify therapeutic leads to reverse CFTR suppression and rescue MCC. TGF-β alters the microRNAome of primary human bronchial epithelium. TGF-β and CS upregulate miR-145-5p expression to suppress CFTR and the CFTR modifier, SLC26A9. miR-145-5p upregulation with a concomitant CFTR and SLC26A9 suppression was validated in CS-exposed mouse models. While miR-145-5p antagonism rescued the effects of TGF-β in bronchial epithelial cells following transfection, an aptamer to block TGF-β signaling rescues CS- and TGF-β-mediated suppression of CFTR biogenesis and function in the absence of any transfection reagent. These results demonstrate that miR-145-5p plays a significant role in acquired CFTR dysfunction by CS, and they validate a clinically feasible strategy for delivery by inhalation to locally modulate TGF-β signaling in the airway and rescue CFTR biogenesis and function.

Indexed as

AnimalsCells, CulturedCystic Fibrosis Transmembrane Conductance RegulatorHumansMiceMice, Mutant StrainsMicroRNAsPulmonary Disease, Chronic ObstructiveReceptor, Transforming Growth Factor-beta Type IIRespiratory MucosaSmokingTransforming Growth Factor betaCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorMicroRNAsMIRN145 microRNA, humanReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor betaCFTRcigarette smokeCOPDmicroRNAomemiR-145-5pSLC26A9TGFBR2TGFBR2 aptamerTGF-β signaling

Identifiers

PMID30595527
PMCPMC6369566
OpenAlexW2902847844

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.