Evidence map›Paper›PMID 25428218›Full record

ArticleBlood2015

The role of galectin-3 and galectin-3-binding protein in venous thrombosis.

Elise P DeRoo, Shirley K Wrobleski, Evelyn M Shea, Ramsey K Al-Khalil, Angela E Hawley, Peter K Henke, Daniel D Myers, Thomas W Wakefield, Jose A Diaz

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.4field-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

60 citing papers in PubMed, 114 citations in OpenAlex.

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  18. Galectin-3-binding protein and future venous thromboembolism.Research and practice in thrombosis and haemostasis · 2024
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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

9 authors at 1 institution in 1 country.

Elise P DeRooDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Shirley K WrobleskiDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Evelyn M SheaDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Ramsey K Al-KhalilDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Angela E HawleyDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Peter K HenkeDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Daniel D MyersDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Thomas W WakefieldDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
Jose A DiazDepartment of Surgery, Section of Vascular Surgery, Conrad Jobst Vascular Research Laboratories, and Unit for Laboratory Animal Research, University of Michigan, Ann Arbor, MI.
University of Michigan–Ann Arbor · US

Funding

Free Radicals Influence the Pathogenesis of Venous ThrombosisK01HL080962 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, DANIEL DURANT · 2007 to 2011
$697k
NHLBI NIH HHS HL080962-01A5NHLBI NIH HHS K01 HL080962
6 · The paper itself

Abstract

Galectin-3-binding protein (gal3bp) and its receptor/ligand, galectin-3 (gal3), are secreted proteins that initiate signaling cascades in several diseases, and recent human proteomic data suggest they may play a role in venous thrombosis (VT). We hypothesized that gal3bp and gal3 may promote VT. Using a mouse stasis model of VT, we found that gal3bp and gal3 were localized on vein wall, red blood cells, platelets, and microparticles, whereas leukocytes expressed gal3 only. Gal3 was dramatically increased during early VT and gal3bp:gal3 colocalized in the leukocyte/endothelial cell interface, where leukocytes were partially attached to the vein wall. Thrombus size correlated with elevated gal3 and interleukin-6 (IL-6) vein wall levels. Recombinant gal3 promoted VT and increased vein wall IL-6 mRNA. Although recombinant gal3 restored the VT size in gal3(-/-) mice, it had no effect on IL6(-/-) mice, suggesting that gal3:gal3bp promotes VT through IL-6. Moreover, significantly fewer activated neutrophils were present in the gal3(-/-) vein walls. In a group of human patients, elevated circulating gal3bp correlated with acute VT. In conclusion, gal3bp:gal3 play a critical role in VT, likely via IL-6 and PMN-mediated thrombotic mechanisms, and may be a potential biomarker in human VT.

Indexed as

AnimalsAntigens, NeoplasmBiomarkersBiomarkers, TumorBlood PlateletsCarrier ProteinsCell MovementChemokine CCL2Disease Models, AnimalEndothelial CellsErythrocytesExtracellular Matrix ProteinsGalectin 3GlycoproteinsHumansInterleukin-6Antigens, NeoplasmBiomarkersBiomarkers, TumorCarrier ProteinsCcl2 protein, mouseChemokine CCL2Extracellular Matrix ProteinsGalectin 3GlycoproteinsInterleukin-6LGALS3BP protein, humanLgals3 protein, mousePpicap protein, mouseRecombinant ProteinsRNA, Messenger

Identifiers

PMID25428218
PMCPMC4357586
OpenAlexW2045357511

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.