Evidence map›Paper›PMID 23499464›Full record

ArticleThe American journal of pathology2013

Novel proteolytic microvesicles released from human macrophages after exposure to tobacco smoke.

Chun-Jun Li, Yu Liu, Yan Chen, Demin Yu, Kevin Jon Williams, Ming-Lin Liu

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

79 citing papers in PubMed, 121 citations in OpenAlex.

  1. Trial
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  7. Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. The emerging role of extracellular vesicles in bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  12. Review
  13. Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Extracellular vesicles and COPD: foe or friend?Journal of nanobiotechnology · 2023
    Review
  20. Article

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Chun-Jun LiSection of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Yu Liu
Yan Chen
Demin Yu
Kevin Jon Williams
Ming-Lin Liu
Temple University · USTianjin Medical University · CN

Funding

Endocytic Trafficking Motifs in Syndecan &LDL receptorR01HL073898 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI WILLIAMS, KEVIN JON · 2005 to 2008
$1.2M
NHLBI NIH HHS R01 HL073898NHLBI NIH HHS R01HL73898
6 · The paper itself

Abstract

Cigarette smoking damages the extracellular matrix in a variety of locations, leading to atherosclerotic plaque instability and emphysematous lung destruction, but the underlying mechanisms remain poorly understood. Here, we sought to determine whether exposure of human macrophages, a key participant in extracellular matrix damage, to tobacco smoke extract (TSE) induces the release of microvesicles (MVs; or microparticles) with proteolytic activity; the major proteases involved; and the cellular mechanisms that might mediate their generation. We found that MVs released from TSE-exposed macrophages carry substantial gelatinolytic and collagenolytic activities that surprisingly can be predominantly attributed to a single transmembrane protease of the matrix metalloproteinase (MMP) superfamily (namely, MMP14). Flow cytometric counts revealed that exposure of human macrophages to TSE for 20 hours more than quadrupled their production of MMP14-positive MVs (control, 1112 ± 231; TSE-induced, 5823 ± 2192 MMP14-positive MVs/μL of conditioned medium; means ± SEM; n = 6; P < 0.01). Our results indicate that the production of these MVs by human macrophages relies on a series of regulated steps that include activation of two mitogen-activated protein kinases (MAPKs, i.e., the Jun N-terminal kinase and p38 MAPK), and then MAPK-dependent induction and maturation of cellular MMP14, a remarkable accumulation of MMP14 into nascent plasma membrane blebs, and finally caspase- and MAPK-dependent apoptosis and apoptotic microvesicle generation. Proteolytically active MVs induced by tobacco smoke may be novel mediators of clinical important matrix destruction in smokers.

Indexed as

ProteolysisSmokingApoptosisCell-Derived MicroparticlesCell LineCell MembraneEnzyme ActivationHumansJNK Mitogen-Activated Protein KinasesMacrophagesMatrix Metalloproteinase 14p38 Mitogen-Activated Protein KinasesJNK Mitogen-Activated Protein KinasesMatrix Metalloproteinase 14MMP14 protein, humanp38 Mitogen-Activated Protein Kinases

Identifiers

PMID23499464
PMCPMC3644720
OpenAlexW2068322460

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.