Evidence map›Paper›PMID 23703615›Full record

ArticleThe Journal of biological chemistry2013

Major vault protein regulates class A scavenger receptor-mediated tumor necrosis factor-α synthesis and apoptosis in macrophages.

Jingjing Ben, Yan Zhang, Rongmei Zhou, Haiyang Zhang, Xudong Zhu, Xiaoyu Li, Hanwen Zhang, Nan Li, Xiaodan Zhou, Hui Bai and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. 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
2.2field-weighted citation impact, top 12% 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.

  1. Review
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  5. Review
  6. Immunoediting role for major vault protein in apoptotic signaling induced by bacterialProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Molecules (Basel, Switzerland) · 2020
    Review
  11. Review
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  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Class A1 scavenger receptors in cardiovascular diseases.British journal of pharmacology · 2015
    Review
  19. 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

14 authors at 3 institutions in 2 countries.

Jingjing BenAtherosclerosis Research Center, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing 210029, China.
Yan Zhang
Rongmei Zhou
Haiyang Zhang
Xudong Zhu
Xiaoyu Li
Hanwen Zhang
Nan Li
Xiaodan Zhou
Hui Bai
Qing Yang
Donghai Li
Yong Xu
Qi Chen
Institute for Atherosclerosis Research · RUNanjing Medical University · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is considered a disease of chronic inflammation largely initiated and perpetuated by macrophage-dependent synthesis and release of pro-inflammatory mediators. Class A scavenger receptor (SR-A) expressed on macrophages plays a key role in this process. However, how SR-A-mediated pro-inflammatory response is modulated in macrophages remains ill defined. Here through immunoprecipitation coupled with mass spectrometry, we reported major vault protein (MVP) as a novel binding partner for SR-A. The interaction between SR-A and MVP was confirmed by immunofluorescence staining and chemical cross-linking assay. Treatment of macrophages with fucoidan, a SR-A ligand, led to a marked increase in TNF-α production, which was attenuated by MVP depletion. Further analysis revealed that SR-A stimulated TNF-α synthesis in macrophages via the caveolin- instead of clathrin-mediated endocytic pathway linked to p38 and JNK, but not ERK, signaling pathways. Importantly, fucoidan invoked an enrichment of MVP in lipid raft, a caveolin-reliant membrane structure, and enhanced the interaction among SR-A, caveolin, and MVP. Finally, we demonstrated that MVP elimination ameliorated SR-A-mediated apoptosis in macrophages. As such, MVP may fine-tune SR-A activity in macrophages which contributes to the development of atherosclerosis.

Indexed as

ApoptosisAnimalsAntineoplastic AgentsAtherosclerosisCaveolinsCells, CulturedClathrinEndocytosisMacrophages, PeritonealMajor Vault ProteinMembrane MicrodomainsMicePolysaccharidesScavenger Receptors, Class ASignal TransductionTumor Necrosis Factor-alphaAntineoplastic AgentsCaveolinsClathrinfucoidanMajor Vault ProteinMsr1 protein, mousePolysaccharidesScavenger Receptors, Class ATumor Necrosis Factor-alphaVault Ribonucleoprotein ParticlesApoptosisCaveolaeMacrophagesMajor Vault ProteinScavenger ReceptorTumor Necrosis Factor (TNF)

Identifiers

PMID23703615
PMCPMC3707704
OpenAlexW2097588082

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.