Evidence map›Paper›PMID 22300502›Full record

ArticleCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

Deletion of tenascin-C gene exacerbates atherosclerosis and induces intraplaque hemorrhage in Apo-E-deficient mice.

Lai Wang, Wei Wang, Prediman K Shah, Lei Song, Mingjie Yang, Behrooz G Sharifi

Abstract read
In one paragraph

Article in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. 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
1.2field-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, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Association ofGenetic testing and molecular biomarkers · 2024
    Article
  4. Article
  5. The role of TNC in atherosclerosis and drug development opportunities.International journal of biological sciences · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Tenascin-c renders a proangiogenic phenotype in macrophage via annexin II.Journal of cellular and molecular medicine · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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

6 authors at 2 institutions in 1 country.

Lai WangOppenheimer Atherosclerosis Research Center and the Division of Cardiology, Cedars Sinai Heart Institute, Los Angeles, CA 90048, USA.
Wei Wang
Prediman K Shah
Lei Song
Mingjie Yang
Behrooz G Sharifi
Cedars-Sinai Medical Center · USCalifornia State Polytechnic University · US

Funding

The Role of Tenascin in Neointimal FormationR01HL050566 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI SHAH, PREDIMAN KRISHAN · 2000 to 2009
$2.7M
PTN FUNCTION IN INTIMAL THICKENINGR01HL104068 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI SHAH, PREDIMAN KRISHAN · 2011 to 2014
$1.6M
Directed Vascular Graft Regeneration in the Mouse Peritoneal CavityR01HL090653 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI SHAH, PREDIMAN KRISHAN, SHARIFI, BEHROOZ G · 2008 to 2011
$1.6M
NHLBI NIH HHS R01 HL050566NHLBI NIH HHS R01 HL090653NHLBI NIH HHS R01 HL104068NHLBI NIH HHS R01 HL50566
6 · The paper itself

Abstract

aimsTenascin-C (TNC), a matricellular protein, is up-regulated in atherosclerotic plaques. We investigated whether the deletion of TNC gene affects the development of atherosclerosis in a murine model.

methodsTNC-/-/apo E-/- mice were generated and used for atherosclerosis studies. We compared these results to those observed in control groups of apo E-/- mice.

resultsThe en face analysis of aortic area showed that the mean aortic lesion area of the double knockout (KO) mice was significantly higher than that of control mice at different times after feeding of atherogenic diet; the accumulation of lesional macrophages and lipids was significantly higher. Analysis of cell adhesion molecules revealed that vascular cell adhesion molecule-1 (VCAM-1), but not intercellular adhesion molecule-1, was up-regulated 1 week after feeding of atherogenic diet in the double KO mouse as compared to apo E-/- mouse. Cell culture studies revealed that the expression of VCAM-1 in endothelial cells isolated from the double KO mouse is more sensitive to the tumor necrosis factor α stimulation than the cells isolated from apo E-/- mice. Cell adhesion studies showed that the adherence of RAW monocytic cells to the endothelial cells was significantly enhanced in the cultured endothelial cells from the TNC gene-deleted cells. Following the prolonged feeding of an atherogenic diet (28-30 weeks), the aortic and carotid atherosclerotic lesions frequently demonstrated large grossly visible areas of intraplaque hemorrhage in the double KO mice compared to control.

conclusionsThese data unveil a protective role for TNC in atherosclerosis and suggest that TNC signaling may have the potential to reduce atherosclerosis, in part by modulating VCAM-1 expression.

Indexed as

Gene DeletionAnimalsAortaApolipoproteins EAtherosclerosisCarotid ArteriesCell AdhesionCells, CulturedDietary FatsDisease Models, AnimalEndothelium, VascularFemaleGenotypeHemorrhageLipoproteinsMaleApolipoproteins EDietary FatsLipoproteinsTenascinVascular Cell Adhesion Molecule-1

Identifiers

PMID22300502
PMCPMC3345312
OpenAlexW2078217356

What OpenQuestion holds

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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.