Evidence map›Paper›PMID 9045878›Full record

ArticleThe Journal of clinical investigation1997

Shear stress induction of the tissue factor gene.

M C Lin, F Almus-Jacobs, H H Chen, G C Parry, N Mackman, J Y Shyy, S Chien

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. 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
9.5field-weighted citation impact, top 1% 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, 236 citations in OpenAlex.

  1. Review
  2. Article
  3. Role of post-translational modifications of Sp1 in cardiovascular diseases.Frontiers in cell and developmental biology · 2024
    Review
  4. Hemostasis and Liver Regeneration.Seminars in thrombosis and hemostasis · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Blood flow modulation of vascular dynamics.Current opinion in lipidology · 2015
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress.American journal of physiology. Heart and circulatory physiology · 2011
    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

7 authors at 3 institutions in 1 country.

M C LinDepartment of Bioengineering and Institute for Biomedical Engineering, University of California, San Diego, La Jolla 92093-0412, USA.
F Almus-Jacobs
H H Chen
G C Parry
N Mackman
J Y Shyy
S Chien
University of California San Diego · USScripps Research Institute · USLa Jolla Bioengineering Institute · US

Funding

MOLECULAR BASIS OF ENDOTHELIAL MECHANICS AND ADHESIONP01HL043026 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SCHMID-SCHOENBEIN, GEERT W. · 1990 to 2005
$8.3M
STUDIES OF ENDOTHELIUM IN RELATION TO ATHEROGENESISR01HL019454 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI CHIEN, SHU · 1985 to 2004
$1.7M
SHEAR STRESS ENHANCEMENT OF SMOOTH MUSCLE CELL MIGRATIONR01HL056707 · NHLBI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI SHYY, JOHN Y-J · 2000 to 2003
$1.4M
MOLECULAR BASIS OF THE ENDOTHELIAL SHEAR STRESS RECEPTORR29HL056707 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SHYY, JOHN Y-J · 1996 to 1999
–
NHLBI NIH HHS HL19454NHLBI NIH HHS HL43026NHLBI NIH HHS HL56707
6 · The paper itself

Abstract

Using flow channel, we report that the application of a laminar shear stress induced a transient increase of tissue factor (TF) procoagulant activity in human umbilical vein endothelial cells (HUVEC), which was accompanied by a rapid and transient induction of the TF mRNA in the HUVEC. Functional analysis of the 2.2 kb TF 5' promoter indicated that a GC-rich region containing three copies each of the EGR-1 and Sp1 sites was required for induction. Mutation of the Sp1 sites, but not the EGR-1 sites, attenuated the response of TF promoter to shear stress. Thus, Sp1 is a newly defined shear stress responsive element. Electrophoretic mobility shift assays showed there was no increase in binding of nuclear extracts from sheared cells to an Sp1 consensus site. In contrast, immunoblotting of these nuclear extracts with antibody against transcription factor Sp1 demonstrated that shear stress increased the phosphorylation of Sp1. We also showed that shear stress, like the phosphatase inhibitor okadaic acid, increased the transcriptional activity of Sp1. These findings suggest that the shear stress induction of TF gene expression is mediated through an increased Sp1 transcriptional activity with a concomitant hyperphosphorylation of Sp1.

Indexed as

Gene Expression RegulationEndothelium, VascularHemorheologyHumansPhosphorylationPromoter Regions, GeneticProtein BindingRNA, MessengerSp1 Transcription FactorThromboplastinTranscription, GeneticUmbilical VeinsRNA, MessengerSp1 Transcription FactorThromboplastin

Identifiers

PMID9045878
PMCPMC507858
OpenAlexW2064150552

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.