Evidence map›Paper›PMID 26729618›Full record

ArticleScientific reports2016

EBP50 induces apoptosis in macrophages by upregulating nitric oxide production to eliminate intracellular Mycobacterium tuberculosis.

Yang Guo, Yating Deng, Zikun Huang, Qing Luo, Yiping Peng, Jie Chen, Hong Jiang, Jianqing Ye, Junming Li

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

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 14 citations in OpenAlex.

  1. Doxycycline Induces Apoptosis ofFrontiers in cellular and infection microbiology · 2021
    Article
  2. Review
  3. 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

9 authors at 3 institutions in 1 country.

Yang GuoDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Yating DengDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Zikun HuangDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Qing LuoDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Yiping PengDepartment of Tuberculosis, Jiangxi Chest Hospital, Nanchang, 330006, China.
Jie ChenDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Hong JiangDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Jianqing YeDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Junming LiDepartment of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Nanchang University · CNFirst Affiliated Hospital of Nanchang University · CNJiangxi Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium bovis BCG is known to have the capacity to inhibit the positioning of iNOS on BCG-containing phagosomes by interfering with EBP50, a scaffolding protein that controls the recruitment of inducible nitric oxide synthase (iNOS) at the vicinity of phagosomes in macrophages. However, knockdown of the expression of EBP50 still facilitates the intracellular survival of BCG, which suggested that EBP50 may have some other unknown antimycobacterial properties. In this study we show that overexpression of EBP50 by a recombinant lentivirus had no effect on the iNOS recruitment to M.tuberculosis-containing phagosomes, but significantly promoted the elimination of intracellular M.tuberculosis. We revealed in the present study that the enhancement of intracellular killing to M. tuberculosis upon EBP50 overexpression was due to the increased level of apoptosis in macrophages. We showed that EBP50 overexpression significantly increased the expression of iNOS and generation of nitric oxide (NO), and EBP50-induced apoptosis was NO-dependent and mediated by Bax and caspase-3. We found that M. tuberculosis decreases while Mycobacterium smegmatis increases the expression of EBP50 in RAW264.7 cells, which suggested that virulent mycobacteria are capable of modulating the antimycobacterial properties of macrophages by inhibiting the expression and interfering with the function of EBP50.

Indexed as

ApoptosisAnimalsbcl-2-Associated X ProteinCaspase 3Cell LineCytotoxicity, ImmunologicFlow CytometryGene Expression RegulationGene Knockdown TechniquesHumansMacrophagesMiceMycobacterium tuberculosisNitric OxideNitric Oxide Synthase Type IIPhagocytosisbcl-2-Associated X ProteinCaspase 3Nitric OxideNitric Oxide Synthase Type IIPhosphoproteinssodium-hydrogen exchanger regulatory factorSodium-Hydrogen Exchangers

Identifiers

PMID26729618
PMCPMC4700441
OpenAlexW2232272726

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.