Evidence map›Paper›PMID 26270571›Full record

ArticlePediatric research2015

Nuclear bioavailability of the glucocorticoid receptor in a pediatric asthma cohort with variable corticosteroid responsiveness.

Salomon Cornejo, Kelan Tantisira, Benjamin A Raby, Scott T Weiss, Feige Kaplan

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Pediatric research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Pharmacogenetics of childhood uncontrolled asthma.Expert review of clinical immunology · 2025
    Review
  3. Review
  4. Th1 cytokines TNF-α and IFN-γ promote corticosteroid resistance in developing human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  5. Review
  6. 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

5 authors at 4 institutions in 2 countries.

Salomon CornejoMcGill University - Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada.
Kelan TantisiraChanning Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Benjamin A RabyChanning Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Scott T WeissChanning Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Feige KaplanMcGill University - Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada.
Harvard University · USBrigham and Women's Hospital · USMcGill University · CAMontreal Children's Hospital · CA

Funding

THE PHARMACOGENETICS OF ASTHMA TREATMENTU01HL065899 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI TANTISIRA, KELAN G, WEISS, SCOTT T · 2000 to 2014
$38.5M
INTEGRATIVE PHARMACOGENOMICS OF LEUKOTRIENE INHIBITION IN ASTHMAR01HL092197 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI TANTISIRA, KELAN G · 2009 to 2013
$3.6M
Canadian Institutes of Health Research 74683NHLBI NIH HHS R01 HL092197NHLBI NIH HHS R01HL092197NHLBI NIH HHS U01 HL065899
6 · The paper itself

Abstract

backgroundDespite the overall effectiveness of glucocorticoids (GCs) in the treatment of asthma, a large proportion of patients do not fully respond to this medication. The objective of the present study was to investigate the potential molecular mechanisms responsible for corticosteroid insensitivity in pediatric asthma.

methodsAsthmatic children were classified as good (GSR) or poor corticosteroid responders (PSR) based on the changes in pulmonary function following GC treatment. Immortalized B-cells derived from patients at two ends of the spectrum of GC responsiveness (five each) were grown in culture and treated with hydrocortisone (10(-6)M). Baseline and temporal changes in GC receptor (GR) protein and mRNA were evaluated by western blot and quantitative reverse transcription PCR respectively. The effect of GC treatment on GR nuclear levels was assessed by western blots.

resultsCells derived from PSR asthmatics displayed lower GR protein levels when compared to GSR. Moreover, in PSR cells GC-induced nuclear translocation of GR was short-lived and homologous downregulation of GR mRNA and protein was faster than in GSR.

conclusionOur data demonstrate the existence of a novel mechanism of GC insensitivity resulting from limited GR nuclear bioavailability as a consequence of decreased baseline GR protein expression and more rapid hormone-induced downregulation.

Indexed as

Active Transport, Cell NucleusAdolescentAnti-Inflammatory AgentsAsthmaB-LymphocytesCell Line, TransformedCell NucleusChildChild, PreschoolDown-RegulationDrug ResistanceFemaleForced Expiratory VolumeHumansHydrocortisoneLungAnti-Inflammatory AgentsHydrocortisoneNR3C1 protein, humanReceptors, GlucocorticoidRNA, Messenger

Identifiers

PMID26270571
OpenAlexW2312470847

What OpenQuestion holds

Textmetadata
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.