Evidence map›Paper›PMID 24172143›Full record

ArticleBritish journal of pharmacology2014

Glucocorticoids suppress hypoxia-induced COX-2 and hypoxia inducible factor-1α expression through the induction of glucocorticoid-induced leucine zipper.

Wonchung Lim, Choa Park, Myeong Kuk Shim, Yong Hee Lee, You Mie Lee, YoungJoo Lee

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

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  12. Glucocorticoid-Dependent Mechanisms of Brain Tolerance to Hypoxia.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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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

6 authors at 2 institutions in 1 country.

Wonchung LimDepartment of Bioscience and Biotechnology, College of Life Science, Institute of Biotechnology, Sejong University, Seoul, Korea.
Choa Park
Myeong Kuk Shim
Yong Hee Lee
You Mie Lee
YoungJoo Lee
Chungbuk National University · KRSejong University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe COX-2/PGE2 pathway in hypoxic cancer cells has important implications for stimulation of inflammation and tumourigenesis. However, the mechanism by which glucocorticoid receptors (GRs) inhibit COX-2 during hypoxia has not been elucidated. Hence, we explored the mechanisms underlying glucocorticoid-mediated inhibition of hypoxia-induced COX-2 in human distal lung epithelial A549 cells. EXPERIMENTAL APPROACH: The expressions of COX-2 and glucocorticoid-induced leucine zipper (GILZ) in A549 cells were determined by Western blot and/or quantitative real time-PCR respectively. The anti-invasive effect of GILZ on A549 cells was evaluated using the matrigel invasion assay. KEY

resultsThe hypoxia-induced increase in COX-2 protein and mRNA levels and promoter activity were suppressed by dexamethasone, and this effect of dexamethasone was antagonized by the GR antagonist RU486. Overexpression of GILZ in A549 cells also inhibited hypoxia-induced COX-2 expression levels and knockdown of GILZ reduced the glucocorticoid-mediated inhibition of hypoxia-induced COX-2 expression, indicating that the inhibitory effects of dexamethasone on hypoxia-induced COX-2 are mediated by GILZ. GILZ suppressed the expression of hypoxia inducible factor (HIF)-1α at the protein level and affected its signalling pathway. Hypoxia-induced cell invasion was also dramatically reduced by GILZ expression. CONCLUSION AND IMPLICATIONS: Dexamethasone-induced upregulation of GILZ not only inhibits the hypoxic-evoked induction of COX-2 expression and cell invasion but further blocks the HIF-1 pathway by destabilizing HIF-1α expression. Taken together, these findings suggest that the suppression of hypoxia-induced COX-2 by glucocorticoids is mediated by GILZ. Hence, GILZ is a potential key therapeutic target for suppression of inflammation under hypoxia.

Indexed as

Alveolar Epithelial CellsAnimalsAnti-Inflammatory Agents, Non-SteroidalCell HypoxiaCell LineCell MovementCyclooxygenase 2DexamethasoneGene Expression RegulationGenes, ReporterGlucocorticoidsHormone AntagonistsHumansHypoxia-Inducible Factor 1, alpha SubunitMiceReceptors, GlucocorticoidAnti-Inflammatory Agents, Non-SteroidalCyclooxygenase 2DexamethasoneGlucocorticoidsHIF1A protein, humanHormone AntagonistsHypoxia-Inducible Factor 1, alpha SubunitPTGS2 protein, humanPtgs2 protein, mouseReceptors, GlucocorticoidTranscription FactorsTSC22D3 protein, humancyclooxygenase-2glucocorticoid-induced leucine zipperglucocorticoid receptorhypoxiahypoxia-inducible factor-1

Identifiers

PMID24172143
PMCPMC3969085
OpenAlexW1593018684

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.