Evidence map›Paper›PMID 28700908›Full record

ArticleBiophysical journal2017

Endothelial Glycocalyx-Mediated Nitric Oxide Production in Response to Selective AFM Pulling.

Anne Marie W Bartosch, Rick Mathews, John M Tarbell

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 104 citations in OpenAlex.

  1. Trial
  2. Review
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  5. Article
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  7. Article
  8. Heparan Sulfates Regulate Vascular Reactivity in Syndecan 1 Knockout Mice.International journal of molecular sciences · 2026
    Article
  9. Endothelial Surface Glycocalyx in Vascular Functions and Diseases.Advances in experimental medicine and biology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Integrating molecular and cellular components of endothelial shear stress mechanotransduction.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  17. Article
  18. Cerebrovascular Endothelial Dysfunction: Role of BACE1.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  19. Review
  20. Review

14 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

3 authors at 1 institution in 1 country.

Anne Marie W BartoschDepartment of Biomedical Engineering, The City College of New York, New York, New York.
Rick MathewsDepartment of Biomedical Engineering, The City College of New York, New York, New York; The William E. Macaulay Honors College, New York, New York.
John M TarbellDepartment of Biomedical Engineering, The City College of New York, New York, New York. Electronic address: jtarbell@ccny.cuny.edu.
City College of New York · US

Funding

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 HL094889
6 · The paper itself

Abstract

Nitric oxide (NO) is a regulatory molecule in the vascular system and its inhibition due to endothelial injury contributes to cardiovascular disease. The glycocalyx is a thin layer of glycolipids, glycoproteins, and proteoglycans on the surface of mammalian epithelial cells. Extracellular forces are transmitted through the glycocalyx to initiate intracellular signaling pathways. In endothelial cells (ECs), previous studies have shown the glycocalyx to be a significant mediator of NO production; degradation of the endothelial glycocalyx layer (EGL) drastically reduces EC production of NO in response to fluid shear stress. However, the specific EGL components involved in this process are not well established. Recent work using short-hairpin RNA approaches in vitro suggest that the proteoglycan glypican-1, not syndecan-1, is the dominant core protein mediating shear-induced NO production. We utilized atomic force microscopy (AFM) to apply force selectively to components of the EGL of confluent rat fat pad ECs (RFPECs), including proteoglycans and glycosaminoglycans, to observe how each component individually contributes to force-induced production of NO. 4,5-diaminofluorescein diacetate, a cell-permeable fluorescent molecule, was used to detect changes in intracellular NO production. Antibody-coated AFM probes exhibited strong surface binding to RFPEC monolayers, with 100-300 pN mean adhesion forces. AFM pulling on glypican-1 and heparan sulfate for 10 min caused significantly increased NO production, whereas pulling on syndecan-1, CD44, hyaluronic acid, and with control probes did not. We conclude that AFM pulling can be used to activate EGL-mediated NO production and that the heparan sulfate proteoglycan glypican-1 is a primary mechanosensor for shear-induced NO production.

Indexed as

Adipose TissueAnimalsEndothelial CellsFluoresceinGlycocalyxGlypicansHeparan SulfateHyaluronan ReceptorsHyaluronic AcidIndicators and ReagentsIntracellular SpaceMechanotransduction, CellularMicroscopy, Atomic ForceNitric OxideRatsStress, Mechanical4,5-diaminofluorescein diacetateFluoresceinGlypicansHeparan SulfateHyaluronan ReceptorsHyaluronic AcidIndicators and ReagentsNitric OxideSdc1 protein, ratSyndecan-1

Identifiers

PMID28700908
PMCPMC5510764
OpenAlexW748827547

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.