Evidence map›Paper›PMID 22940282›Full record

ArticleVascular pharmacology2013

Nicotinic acetylcholine receptor mediates nicotine-induced actin cytoskeletal remodeling and extracellular matrix degradation by vascular smooth muscle cells.

Zhizhan Gu, Vera Fonseca, Chi-Ming Hai

Open access · greenAbstract readComparative Study
In one paragraph

Article in Vascular pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Adverse Effects of Nicotine on Human Sperm Nuclear Proteins.The world journal of men's health · 2025
    Review
  5. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Review
  7. Nicotine and vascular dysfunction.Acta physiologica (Oxford, England) · 2021
    Review
  8. Smoking and the Pathophysiology of Peripheral Artery Disease.Frontiers in cardiovascular medicine · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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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 2 institutions in 1 country.

Zhizhan GuDivision of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Vera Fonseca
Chi-Ming Hai
John Brown University · USBrigham and Women's Hospital · US

Funding

Mechanosensitive Modulation of Airway ContractionR56HL052714 · NHLBI · BROWN UNIVERSITY · PI HAI, CHI-MING · 2008 to 2008
$330k
NHLBI NIH HHS R56 HL052714NHLBI NIH HHS R56-HL-52714
6 · The paper itself

Abstract

Cigarette smoking is a significant risk factor for atherosclerosis, which involves the invasion of vascular smooth muscle cells (VSMCs) from the media to intima. A hallmark of many invasive cells is actin cytoskeletal remodeling in the form of podosomes, accompanied by extracellular matrix (ECM) degradation. A7r5 VSMCs form podosomes in response to PKC activation. In this study, we found that cigarette smoke extract, nicotine, and the cholinergic agonist, carbachol, were similarly effective in inducing the formation of podosome rosettes in A7r5 VSMCs. α-Bungarotoxin and atropine experiments confirmed the involvement of nicotinic acetylcholine receptors (nAChRs). Western blotting and immunofluorescence experiments revealed the aggregation of nAChRs at podosome rosettes. Cycloheximide experiments and media exchange experiments suggested that autocrine factor(s) and intracellular phenotypic modulation are putative mechanisms. In situ zymography experiments indicated that, in response to PKC activation, nicotine-treated cells degraded ECM near podosome rosettes, and possibly endocytose ECM fragments to intracellular compartments. Invasion assay of human aortic smooth muscle cells indicated that nicotine and PKC activation individually and synergistically enhanced cell invasion through ECM. Results from this study suggest that nicotine enhances the ability of VSMCs to degrade and invade ECM. nAChR activation, actin cytoskeletal remodeling and phenotypic modulation are possible mechanisms.

Indexed as

Actin CytoskeletonAnimalsAortaBlotting, WesternCarbacholCells, CulturedExtracellular MatrixFluorescent Antibody TechniqueHumansMuscle, Smooth, VascularMyocytes, Smooth MuscleNicotianaNicotineProtein Kinase CRatsReceptors, NicotinicCarbacholNicotineProtein Kinase CReceptors, NicotinicSmoke

Identifiers

PMID22940282
PMCPMC3530635
OpenAlexW1980272190

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.