Evidence map›Paper›PMID 19929007›Full record

ArticleBiochemistry2010

Control of integrin alphaIIb beta3 outside-in signaling and platelet adhesion by sensing the physical properties of fibrin(ogen) substrates.

Nataly P Podolnikova, Ivan S Yermolenko, Alexander Fuhrmann, Valeryi K Lishko, Sergei Magonov, Benjamin Bowen, Joerg Enderlein, Andriy V Podolnikov, Robert Ros, Tatiana P Ugarova

Abstract read
In one paragraph

Article in Biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Conformational response of αStructure (London, England : 1993) · 2025
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  11. Wdr-1 is essential for F-actin interaction with focal adhesions in platelets.Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis · 2018
    Article
  12. Article
  13. Article
  14. Platelet mechanosensing of substrate stiffness during clot formation mediates adhesion, spreading, and activation.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  15. Article
  16. 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

10 authors at 3 institutions in 2 countries.

Nataly P PodolnikovaCenter for Metabolic Biology, Arizona State University, Tempe, Arizona 85287, USA.
Ivan S Yermolenko
Alexander Fuhrmann
Valeryi K Lishko
Sergei Magonov
Benjamin Bowen
Joerg Enderlein
Andriy V Podolnikov
Robert Ros
Tatiana P Ugarova
Agilent Technologies (United States) · USArizona State University · USUniversity of Göttingen · DE

Funding

The role of beta 2 integrins in macrophage fusionR01HL063199 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI Tatiana P Ugarova · 1999 to 2026
$8.6M
NHLBI NIH HHS R01 HL063199
6 · The paper itself

Abstract

The physical properties of substrates are known to control cell adhesion via integrin-mediated signaling. Fibrin and fibrinogen, the principal components of hemostatic and pathological thrombi, may represent biologically relevant substrates whose variable physical properties control adhesion of leukocytes and platelets. In our previous work, we have shown that binding of fibrinogen to the surface of fibrin clot prevents cell adhesion by creating an antiadhesive fibrinogen layer. Furthermore, fibrinogen immobilized on various surfaces at high density supports weak cell adhesion whereas at low density it is highly adhesive. To explore the mechanism underlying differential cell adhesion, we examined the structural and physical properties of surfaces prepared by deposition of various concentrations of fibrinogen using atomic force microscopy and force spectroscopy. Fibrinogen deposition at high density resulted in an aggregated multilayered material characterized by low adhesion forces. In contrast, immobilization of fibrinogen at low density produced a single layer in which molecules were directly attached to the solid surface, resulting in higher adhesion forces. Consistent with their distinct physical properties, low- but not high-density fibrinogen induced strong alpha(IIb)beta(3)-mediated outside-in signaling in platelets, resulting in their spreading. Moreover, while intact fibrin gels induced strong signaling in platelets, deposition of fibrinogen on the surface of fibrin resulted in diminished cell signaling. The data suggest that deposition of a multilayered fibrinogen matrix prevents stable cell adhesion by modifying the physical properties of surfaces, which results in reduced force generation and insufficient signaling. The mechanism whereby circulating fibrinogen alters adhesive properties of fibrin clots may have important implications for control of thrombus formation and thrombogenicity of biomaterials.

Indexed as

Signal TransductionBinding SitesBlood PlateletsCell AdhesionCytoplasmFibrinFibrinogenHumansMicroscopy, Atomic ForceMicroscopy, Electron, ScanningPlatelet AdhesivenessPlatelet Glycoprotein GPIIb-IIIa ComplexSurface PropertiesFibrinFibrinogenPlatelet Glycoprotein GPIIb-IIIa Complex

Identifiers

PMID19929007
PMCPMC4530791
OpenAlexW2123122212

What OpenQuestion holds

Textmetadata
LicenceTDM
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.