Evidence map›Paper›PMID 26384220›Full record

ArticleJournal of innate immunity2016

Glucocorticoid-Induced Leucine Zipper Is Expressed in Human Neutrophils and Promotes Apoptosis through Mcl-1 Down-Regulation.

Marie-Alix Espinasse, Aurélie Pépin, Pauline Virault-Rocroy, Natacha Szely, Sylvie Chollet-Martin, Marc Pallardy, Armelle Biola-Vidamment

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  16. Article
  17. How Glucocorticoids Affect the Neutrophil Life.International journal of molecular sciences · 2018
    Review
  18. Article
  19. Dexamethasone Stimulates Hepatitis B Virus (HBV) Replication Through Autophagy.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  20. Review
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 2 institutions in 1 country.

Marie-Alix EspinasseUMR996 - Inflammation, Chemokines and Immunopathology, Inserm, Universitx00E9; Paris-Sud, Universitx00E9; Paris-Saclay, Chx00E2;tenay-Malabry, France.
Aurélie Pépin
Pauline Virault-Rocroy
Natacha Szely
Sylvie Chollet-Martin
Marc Pallardy
Armelle Biola-Vidamment
Inserm · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein, the expression of which is mainly induced by glucocorticoids (GCs) in haematopoietic cells. GILZ regulates signal transduction pathways of inflammation and plays a role in cell survival. The objective of this study was to evaluate the expression and mechanisms of action of GILZ in the apoptosis of human neutrophils. GILZ expression was induced by GCs in human neutrophils, enhanced upon phosphatidylinositol 3-kinase inhibition and resulted in apoptosis amplification. We then stably transfected PLB-985 cells with the human gilz gene and differentiated both control and GILZ-overexpressing clones in neutrophil-like cells. GILZ overexpression in PLB-985 cells led to an exacerbated apoptosis, associated with caspase-3, caspase-9 and caspase-8 activations, and a loss of mitochondrial potential, suggesting that GILZ-induced apoptosis used the mitochondrial pathway. The expression of BH3 interacting domain death agonist, Bcl-2 interacting mediator of cell death, annexin-A1 and Bcl-2-associated X was not affected in PLB-985-GILZ clones, but phosphorylation and subsequent proteasomal degradation of myeloid cell leukemia-1 (Mcl-1) were observed. Noteworthy, Mcl-1 phosphorylation was related to a significant and sustained activation of c-Jun N-terminal kinase (JNK) in PLB-985-GILZ clones. These results reveal GILZ to be a new actor in apoptosis regulation in neutrophil-like cells involving JNK and Mcl-1.

Indexed as

ApoptosisCaspasesCell DifferentiationCell Line, TumorDown-RegulationGlucocorticoidsHumansInflammationJNK Mitogen-Activated Protein KinasesMembrane Potential, MitochondrialMitochondriaMyeloid Cell Leukemia Sequence 1 ProteinNeutrophilsPhosphatidylinositol 3-KinasesPhosphorylationProteasome Endopeptidase ComplexCaspasesGlucocorticoidsJNK Mitogen-Activated Protein KinasesMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-KinasesProteasome Endopeptidase ComplexTranscription FactorsTSC22D3 protein, human

Identifiers

PMID26384220
PMCPMC6738861
OpenAlexW1949260419

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.