Evidence map›Paper›PMID 26212910›Full record

ArticleThe American journal of pathology2015

αvβ3 Integrins Mediate Flow-Induced NF-κB Activation, Proinflammatory Gene Expression, and Early Atherogenic Inflammation.

Jie Chen, Jonette Green, Arif Yurdagul, Patrick Albert, Marshall C McInnis, A Wayne Orr

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

62 citing papers in PubMed, 100 citations in OpenAlex.

  1. THSD7A Exacerbates Atherosclerosis via Activation of Signaling Axis αvβ3/CEBPD/IL1A.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Mechanism of Bile Acid in Regulating Platelet Function and Thrombotic Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  16. Article
  17. Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024
    Review
  18. Spatial Mechano-Signaling Regulation of GTPases through Non-Degradative Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  19. Review
  20. Review

2 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jie ChenDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana.
Jonette GreenDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana.
Arif YurdagulDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana; Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, Louisiana.
Patrick AlbertDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana.
Marshall C McInnisDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana.
A Wayne OrrDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana. Electronic address: aorr@lsuhsc.edu.
Louisiana State University Health Sciences Center Shreveport · US

Funding

Matrix Signaling in Endothelial Cell DysfunctionR01HL098435 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2010 to 2020
$3.2M
NHLBI NIH HHS R01 HL098435
6 · The paper itself

Abstract

Endothelial cell interactions with transitional matrix proteins, such as fibronectin, occur early during atherogenesis and regulate shear stress-induced endothelial cell activation. Multiple endothelial cell integrins bind transitional matrix proteins, including α5β1, αvβ3, and αvβ5. However, the role these integrins play in mediating shear stress-induced endothelial cell activation remains unclear. Therefore, we sought to elucidate which integrin heterodimers mediate shear stress-induced endothelial cell activation and early atherogenesis. We now show that inhibiting αvβ3 integrins (S247, siRNA), but not α5β1 or αvβ5, blunts shear stress-induced proinflammatory signaling (NF-κB, p21-activated kinase) and gene expression (ICAM1, VCAM1). Importantly, inhibiting αvβ3 did not affect cytokine-induced proinflammatory responses or inhibit all shear stress-induced signaling, because Akt, endothelial nitric oxide synthase, and extracellular regulated kinase activation remained intact. Furthermore, inhibiting αv integrins (S247), but not α5 (ATN-161), in atherosclerosis-prone apolipoprotein E knockout mice significantly reduced vascular remodeling after acute induction of disturbed flow. S247 treatment similarly reduced early diet-induced atherosclerotic plaque formation associated with both diminished inflammation (expression of vascular cell adhesion molecule 1, plaque macrophage content) and reduced smooth muscle incorporation. Inducible, endothelial cell-specific αv integrin deletion similarly blunted inflammation in models of disturbed flow and diet-induced atherogenesis but did not affect smooth muscle incorporation. Our studies identify αvβ3 as the primary integrin heterodimer mediating shear stress-induced proinflammatory responses and as a key contributor to early atherogenic inflammation.

Indexed as

AnimalsAtherosclerosisCells, CulturedEndothelial CellsGene ExpressionInflammationIntegrin alphaVbeta3MaleMice, KnockoutNF-kappa BSignal TransductionStress, MechanicalVascular Cell Adhesion Molecule-1Integrin alphaVbeta3NF-kappa BVascular Cell Adhesion Molecule-1

Identifiers

PMID26212910
PMCPMC4597278
OpenAlexW1862715758

What OpenQuestion holds

Textmetadata
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.