Evidence map›Paper›PMID 20808940›Full record

ArticlePloS one2010

Shear stress modulation of smooth muscle cell marker genes in 2-D and 3-D depends on mechanotransduction by heparan sulfate proteoglycans and ERK1/2.

Zhong-Dong Shi, Giya Abraham, John M Tarbell

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. On the examination of the viscous response of the brachial artery during flow-mediated dilation.Journal of the mechanical behavior of biomedical materials · 2022
    Article
  7. Article
  8. Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis.International journal of molecular sciences · 2021
    Review
  9. Review
  10. On the modeling of mechanotransduction in flow-mediated dilation.Journal of the mechanical behavior of biomedical materials · 2021
    Article
  11. Biomechanical signal communication in vascular smooth muscle cells.Journal of cell communication and signaling · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
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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

3 authors at 1 institution in 1 country.

Zhong-Dong ShiDepartment of Biomedical Engineering, The City College of New York, The City University of New York, New York, New York, United States of America. zdshi@hotmail.com
Giya Abraham
John M Tarbell
City College of New York · US

Funding

SHEAR STRESS EFFECTS ON ENDOTHELIAL TRANSPORTR01HL057093 · NHLBI · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI TARBELL, JOHN M · 1997 to 2010
$2.7M
The Endothelial Glycocalyx: Its Structure and Function and as a MechanotransducerR01HL094889 · NHLBI · CITY COLLEGE OF NEW YORK · PI TARBELL, JOHN M · 2010 to 2014
$2.4M
NHLBI NIH HHS R01 HL057093NHLBI NIH HHS R01 HL 094889NHLBI NIH HHS R01 HL094889NHLBI NIH HHS R01 HL 57093
6 · The paper itself

Abstract

backgroundDuring vascular injury, vascular smooth muscle cells (SMCs) and fibroblasts/myofibroblasts (FBs/MFBs) are exposed to altered luminal blood flow or transmural interstitial flow. We investigate the effects of these two types of fluid flows on the phenotypes of SMCs and MFBs and the underlying mechanotransduction mechanisms. METHODOLOGY/PRINCIPAL

findingsExposure to 8 dyn/cm(2) laminar flow shear stress (2-dimensional, 2-D) for 15 h significantly reduced expression of alpha-smooth muscle actin (alpha-SMA), smooth muscle protein 22 (SM22), SM myosin heavy chain (SM-MHC), smoothelin, and calponin. Cells suspended in collagen gels were exposed to interstitial flow (1 cmH(2)O, approximately 0.05 dyn/cm(2), 3-D), and after 6 h of exposure, expression of SM-MHC, smoothelin, and calponin were significantly reduced, while expression of alpha-SMA and SM22 were markedly enhanced. PD98059 (an ERK1/2 inhibitor) and heparinase III (an enzyme to cleave heparan sulfate) significantly blocked the effects of laminar flow on gene expression, and also reversed the effects of interstitial flow on SM-MHC, smoothelin, and calponin, but enhanced interstitial flow-induced expression of alpha-SMA and SM22. SMCs and MFBs have similar responses to fluid flow. Silencing ERK1/2 completely blocked the effects of both laminar flow and interstitial flow on SMC marker gene expression. Western blotting showed that both types of flows induced ERK1/2 activation that was inhibited by disruption of heparan sulfate proteoglycans (HSPGs). CONCLUSIONS/SIGNIFICANCE: The results suggest that HSPG-mediated ERK1/2 activation is an important mechanotransduction pathway modulating SMC marker gene expression when SMCs and MFBs are exposed to flow. Fluid flow may be involved in vascular remodeling and lesion formation by affecting phenotypes of vascular wall cells. This study has implications in understanding the flow-related mechanobiology in vascular lesion formation, tumor cell invasion, and stem cell differentiation.

Indexed as

Mechanotransduction, CellularStress, MechanicalAnimalsBiomarkersBiomechanical PhenomenaFlavonoidsGene Expression RegulationGene Knockdown TechniquesHeparan Sulfate ProteoglycansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocytes, Smooth MusclePhenotypePolysaccharide-LyasesRats2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneBiomarkersFlavonoidsHeparan Sulfate Proteoglycansheparitinsulfate lyaseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Polysaccharide-Lyases

Identifiers

PMID20808940
PMCPMC2922372
OpenAlexW1995981837

What OpenQuestion holds

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LicenceCC BY
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.