Evidence map›Paper›PMID 31064000›Full record

ArticleJournal of vascular research2019

Cigarette Smoke Extract Activates Tartrate-Resistant Acid Phosphatase-Positive Macrophage.

Kimihiro Igari, Matthew J Kelly, Dai Yamanouchi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of vascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Unpacking the Complexities of a Silent Killer.International journal of molecular sciences · 2023
    Article
  2. Article
  3. Article
  4. Smoking and the Pathophysiology of Peripheral Artery Disease.Frontiers in cardiovascular medicine · 2021
    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

3 authors at 1 institution in 1 country.

Kimihiro IgariDivision of Vascular Surgery, Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Matthew J KellyDivision of Vascular Surgery, Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Dai YamanouchiDivision of Vascular Surgery, Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA, yamano@surgery.wisc.edu.
University of Wisconsin–Madison · US

Funding

Vascular Surgery Research Training ProgramT32HL110853 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MATSUMURA, JON STEVEN · 2012 to 2021
$2.6M
American Heart Association-American Stroke Association 17GRNT33671064NHLBI NIH HHS T32 HL110853
6 · The paper itself

Abstract

backgroundIt has been reported that smoking is one of the strongest positive risk factors for abdominal aortic aneurysms (AAAs). Although many studies have been directed to decipher the effect of smoking on AAA, its effect on macrophage activation has not yet been explored.

objectivesWe have reported the importance of osteoclastogenesis (OCG) in aneurysm formation. Therefore, we examined the effect of cigarette smoking on OCG and arterial aneurysmal formation by using cigarette smoke extract (CSE) in this study.

methodsMacrophage cell lines were stimulated with CSE, and their activation and differentiation were examined in vitro. Since macrophages activated through the OCG pathway are identified by tartrate-resistant acid phosphatase (TRAP) expression, these cells are referred to as TRAP-positive macrophages (TPMs) in this study. We also applied CSE-contained PBS in the calcium chloride-induced mouse carotid aneurysm model in vivo.

resultsMacrophages stimulated with CSE expressed significantly higher levels of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), TRAP, cathepsin K, matrix metalloproteinase-9 and membrane-type metalloproteinase (MT1-MMP). CSE-treated mouse aneurysms showed increased aneurysm size with increased TPM infiltration and protease expression compared to non-CSE-treated mouse aneurysms.

conclusionsThese results suggest that CSE intensifies OCG in macrophages and promotes arterial aneurysmal progression.

Indexed as

AneurysmAnimalsCalcium ChlorideCarotid Artery DiseasesCathepsin KDisease Models, AnimalMacrophage ActivationMacrophagesMaleMatrix Metalloproteinase 9MiceMice, Inbred C57BLOsteoclastsOsteogenesisRAW 264.7 CellsSignal TransductionCalcium ChlorideCathepsin KCtsk protein, mouseMatrix Metalloproteinase 9Mmp9 protein, mouseSmokeTartrate-Resistant Acid PhosphataseAneurysmCigarette smoke extractOsteoclastogenesisTartrate-resistant acid phosphataseTartrate-resistant acid phosphatase-positive macrophage

Identifiers

PMID31064000
PMCPMC6764454
OpenAlexW2944521030

What OpenQuestion holds

Textmetadata
LicenceTDM
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.