Evidence map›Paper›PMID 19047056›Full record

ArticleThe Journal of biological chemistry2009

Biomechanical Regulation of Endothelium-dependent Events Critical for Adaptive Remodeling.

Peter J Mack, Yuzhi Zhang, Seok Chung, Vernella Vickerman, Roger D Kamm, Guillermo García-Cardeña

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The Roles of AMPK in Revascularization.Cardiology research and practice · 2020
    Review
  5. Review
  6. Article
  7. Fluid shear stress upregulates placental growth factor in the vessel wall via NADPH oxidase 4.American journal of physiology. Heart and circulatory physiology · 2015
    Article
  8. Article
  9. Review
  10. Review
  11. The role of shear-induced transforming growth factor-β signaling in the endothelium.Arteriosclerosis, thrombosis, and vascular biology · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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 3 institutions in 1 country.

Peter J MackCenter for Excellence in Vascular Biology, Departments of Pathology, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Yuzhi Zhang
Seok Chung
Vernella Vickerman
Roger D Kamm
Guillermo García-Cardeña
Massachusetts Institute of Technology · USHarvard University · USBrigham and Women's Hospital · US

Funding

NUCLEAR FACTOR KAPPA BETA AND THE INITIATION OF THE ATHEROSCLEROTIC LESIONP50HL056985 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GANZ, PETER · 1997 to 2006
$14.1M
Self-Assembling Peptides for Tissue EngineeringR01EB003805 · NIBIB · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GRODZINSKY, ALAN J. · 2005 to 2009
$6.5M
Molecular, Cell and Tissue Biomechanics Training GrantT32EB006348 · NIBIB · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KAMM, ROGER D · 2006 to 2010
$1.6M
NHLBI NIH HHS P50-HL56985NHLBI NIH HHS R01-HL7066686NIBIB NIH HHS BRP-EB003805NIBIB NIH HHS T32 EB006348
6 · The paper itself

Abstract

Alterations in hemodynamic shear stress acting on the vascular endothelium are critical for adaptive arterial remodeling. The molecular mechanisms regulating this process, however, remain largely uncharacterized. Here, we sought to define the responses evoked in endothelial cells exposed to shear stress waveforms characteristic of coronary collateral vessels and the subsequent paracrine effects on smooth muscle cells. A lumped parameter model of the human coronary collateral circulation was used to simulate normal and adaptive remodeling coronary collateral shear stress waveforms. These waveforms were then applied to cultured human endothelial cells (EC), and the resulting differences in EC gene expression were assessed by genome-wide transcriptional profiling to identify genes distinctly regulated by collateral flow. Analysis of these transcriptional programs identified several genes to be differentially regulated by collateral flow, including genes important for endothelium-smooth muscle interactions. In particular, the transcription factor KLF2 was up-regulated by the adaptive remodeling coronary collateral waveform, and several of its downstream targets displayed the expected modulation, including the down-regulation of connective tissue growth factor. To assess the effect of endothelial KLF2 expression on smooth muscle cell migration, a three-dimensional microfluidic assay was developed. Using this three-dimensional system, we showed that KLF2-expressing EC co-cultured with SMC significantly reduce SMC migration compared with control EC and that this reduction can be rescued by the addition of exogenous connective tissue growth factor. Collectively, these results demonstrate that collateral flow evokes distinct EC gene expression profiles and functional phenotypes that subsequently influence vascular events important for adaptive remodeling.

Indexed as

Models, CardiovascularBlood Flow VelocityCell MovementCells, CulturedCoronary CirculationCoronary VesselsEndothelial CellsGene Expression RegulationHemodynamicsHumansKruppel-Like Transcription FactorsMuscle, Smooth, VascularMyocytes, Smooth MuscleStress, PhysiologicalKLF2 protein, humanKruppel-Like Transcription Factors

Identifiers

PMID19047056
PMCPMC2659199
OpenAlexW2059417573

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.