Cited by 204Fatty Acid Research and HealthAtherosclerosis and Cardiovascular DiseasesEicosanoids and Hypertension Pharmacology

Aspirin-Triggered Lipoxin and Resolvin E1 Modulate Vascular Smooth Muscle Phenotype and Correlate with Peripheral Atherosclerosis

Open access
Ho, Karen J., Spite, Matthew, Owens, Christopher D., Lancero, Hope, Kroemer, Alex H.K., Pande, Reena, Creager, Mark A., Serhan, Charles N. +1 more·2010·The American Journal of Pathology

Abstract

Atherosclerosis is a chronic inflammatory disease of the vessel wall. Recent evidence suggests that chronic vascular inflammation ensues as an imbalance between pro- and anti-inflammatory mediators. Recently identified lipid mediators (eg, lipoxins and resolvins) play active roles in promoting the resolution of inflammation. Alterations in vascular smooth muscle cell (VSMC) phenotype, which manifest as a loss of contractile protein expression and increased proliferation and migration, are prominent mechanistic features of both atherosclerosis and restenosis following various interventions (eg, angioplasty and bypass grafting). We sought to determine whether human atherosclerosis is associated with a "resolution deficit" and whether lipoxins and resolvins influence VSMC phenotype. Here we report that plasma levels of aspirin-triggered lipoxin are significantly lower in patients with symptomatic peripheral artery disease than in healthy volunteers. Both aspirin-triggered lipoxin and resolvin E1 block platelet-derived growth factor-stimulated migration of human saphenous vein SMCs and decrease phosphorylation of the platelet-derived growth factor receptor-β. Importantly, receptors for aspirin-triggered lipoxin and resolvin E1 (ALX and ChemR23, respectively) were identified in human VSMCs. Overall, these results demonstrate that stimulatory lipid mediators confer a protective phenotypic switch in VSMCs and elucidate new functions for these mediators in the regulation of SMC biology. These results also suggest that peripheral artery disease is associated with an inflammation-resolution deficit and highlight a potential therapeutic opportunity for the regulation of vascular injury responses.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.2353/ajpath.2010.091082

Cites

31 of 31 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Lesional macrophages are the principal target of Ac2-26 in these studies, although SPMs might also interact with lesional smooth muscle cells and endothelial cells.

    “Although the above data suggest that lesional macrophages are the principal target of Ac2–26 in these studies, SPMs might also interact with lesional smooth muscle cells and endothelial cells107,110.”
  • Plasma levels of LXA4 are decreased in patients with peripheral artery disease compared with healthy controls.

    “Plasma levels of another 5-LOX-derived SPM, LXA4, are decreased in patients with peripheral artery disease compared with healthy controls107.”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Serhan CN, Hong S, Gronert K, Colgan SP, Devchand PR, Mirick G, Moussignac RL: Resolvins: a family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammation signals. J Exp Med 2002, 196:1025-1037

Cited by

Sorted by citations

Authors
Ho, K. J., Spite, M., Owens, C. D., Lancero, H., Kroemer, A. H. K., Pande, R., Creager, M. A., Serhan, C. N., & Conte, M. S.
Affiliations
  • Brigham and Women's Hospital (US)
  • University of California, San Francisco (US)
  • Beth Israel Deaconess Medical Center (US)
Corresponding author
Conte, Michael S.
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2010-10
Volume
177
Issue
4
Pages
2116-2123
ISSN
0002-9440 (ISSN-L)
OpenAlex
W2003076495
Cited by
204
References
31
Citations by year
2026: 5 · 2025: 3 · 2024: 14 · 2023: 13 · 2022: 17 · 2021: 14 · 2020: 10 · 2019: 16 · 2018: 18 · 2017: 15 · 2016: 16 · 2015: 15 · 2014: 13 · 2013: 14 · 2012: 10
FWCI
10.62
Type
journal article
Language
en
Open access
Locations
  • American Journal Of Pathology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health (HL087526, HL75771, K23 HL-92163, P20-RR024489, P50-DE016191)
Topics
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
aspirin-triggered lipoxins, resolvin E1, vascular smooth muscle cells, peripheral arterial disease, atherosclerosis, inflammation resolution, PDGFRβ, ChemR23, smooth muscle cell migration, vascular inflammation, lipid mediators
MeSH terms
Aged, Anti-Inflammatory Agents, Aspirin, Cell Survival, Chemotaxis, Female, Flow Cytometry, Humans, Immunoenzyme Techniques, Male, Middle Aged, Muscle, Smooth, Vascular, Phenotype, Phosphorylation, Platelet-Derived Growth Factor, Prospective Studies, RNA, Messenger, Saphenous Vein, Eicosapentaenoic Acid, Blotting, Western, Case-Control Studies, Receptors, Platelet-Derived Growth Factor, Receptors, Chemokine, Reverse Transcriptase Polymerase Chain Reaction, Lipoxins, Adaptor Proteins, Signal Transducing, Atherosclerosis, Peripheral Arterial Disease

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review