Evidence map›Paper›PMID 24260297›Full record

ArticlePloS one2013

Periostin links mechanical strain to inflammation in abdominal aortic aneurysm.

Osamu Yamashita, Koichi Yoshimura, Ayako Nagasawa, Koshiro Ueda, Noriyasu Morikage, Yasuhiro Ikeda, Kimikazu Hamano

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Periostin in Osteoporosis and Cardiovascular Disease.Journal of the Endocrine Society · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. A Novel Hybrid Drug Delivery System for Treatment of Aortic Aneurysms.International journal of molecular sciences · 2020
    Article
  16. FAK Family Kinases in Vascular Diseases.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. 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

7 authors.

Osamu YamashitaDepartment of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Koichi Yoshimura
Ayako Nagasawa
Koshiro Ueda
Noriyasu Morikage
Yasuhiro Ikeda
Kimikazu Hamano

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAbdominal aortic aneurysms (AAAs) are characterized by chronic inflammation, which contributes to the pathological remodeling of the extracellular matrix. Although mechanical stress has been suggested to promote inflammation in AAA, the molecular mechanism remains uncertain. Periostin is a matricellular protein known to respond to mechanical strain. The aim of this study was to elucidate the role of periostin in mechanotransduction in the pathogenesis of AAA. METHODS AND

resultsWe found significant increases in periostin protein levels in the walls of human AAA specimens. Tissue localization of periostin was associated with inflammatory cell infiltration and destruction of elastic fibers. We examined whether mechanical strain could stimulate periostin expression in cultured rat vascular smooth muscle cells. Cells subjected to 20% uniaxial cyclic strains showed significant increases in periostin protein expression, focal adhesion kinase (FAK) activation, and secretions of monocyte chemoattractant protein-1 (MCP-1) and the active form of matrix metalloproteinase (MMP)-2. These changes were largely abolished by a periostin-neutralizing antibody and by the FAK inhibitor, PF573228. Interestingly, inhibition of either periostin or FAK caused suppression of the other, indicating a positive feedback loop. In human AAA tissues in ex vivo culture, MCP-1 secretion was dramatically suppressed by PF573228. Moreover, in vivo, periaortic application of recombinant periostin in mice led to FAK activation and MCP-1 upregulation in the aortic walls, which resulted in marked cellular infiltration.

conclusionOur findings indicated that periostin plays an important role in mechanotransduction that maintains inflammation via FAK activation in AAA.

Indexed as

AgedAnimalsAorta, AbdominalAortic Aneurysm, AbdominalCell Adhesion MoleculesCells, CulturedChemokine CCL2FemaleFocal Adhesion Kinase 1HumansInflammationMaleMatrix Metalloproteinase 2MiceMice, Inbred C57BLMuscle, Smooth, VascularCell Adhesion MoleculesChemokine CCL2Focal Adhesion Kinase 1Matrix Metalloproteinase 2

Identifiers

PMID24260297
PMCPMC3833967

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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.