Evidence map›Paper›PMID 26676803›Full record

ArticleThrombosis and haemostasis2016

Developmental endothelial locus-1 modulates platelet-monocyte interactions and instant blood-mediated inflammatory reaction in islet transplantation.

Ioannis Kourtzelis, Klara Kotlabova, Jong-Hyung Lim, Ioannis Mitroulis, Anaisa Ferreira, Lan-Sun Chen, Bettina Gercken, Anja Steffen, Elisabeth Kemter, Anne Klotzsche-von Ameln and 7 more

Open access · greenAbstract read
In one paragraph

Article in Thrombosis and haemostasis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  18. Regulation of c-Jun NHJournal of clinical medicine · 2019
    Review
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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

17 authors at 1 institution in 1 country.

Ioannis KourtzelisDr. Ioannis Kourtzelis, Department of Clinical Pathobiochemistry, Medical Faculty, Technische Universität Dresden, Fetscherstraße 74, 01307 Dresden, Germany, Tel.: +49 351 4586250, E-mail: Iannis.Kourtzelis@uniklinikum-dresden.de.
Klara Kotlabova
Jong-Hyung Lim
Ioannis Mitroulis
Anaisa Ferreira
Lan-Sun Chen
Bettina Gercken
Anja Steffen
Elisabeth Kemter
Anne Klotzsche-von Ameln
Claudia Waskow
Kavita Hosur
Antonios Chatzigeorgiou
Barbara Ludwig
Eckhard Wolf
George Hajishengallis
Triantafyllos Chavakis
Technische Universität Dresden · DE

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
Del-1: Molecular and Cellular Targets in PeriodontitisR01DE024716 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2015 to 2019
$2.0M
NIAID NIH HHS AI068730NIAID NIH HHS P01 AI068730NIDCR NIH HHS DE024716NIDCR NIH HHS R01 DE024716
6 · The paper itself

Abstract

Platelet-monocyte interactions are strongly implicated in thrombo-inflammatory injury by actively contributing to intravascular inflammation, leukocyte recruitment to inflamed sites, and the amplification of the procoagulant response. Instant blood-mediated inflammatory reaction (IBMIR) represents thrombo-inflammatory injury elicited upon pancreatic islet transplantation (islet-Tx), thereby dramatically affecting transplant survival and function. Developmental endothelial locus-1 (Del-1) is a functionally versatile endothelial cell-derived homeostatic factor with anti-inflammatory properties, but its potential role in IBMIR has not been previously addressed. Here, we establish Del-1 as a novel inhibitor of IBMIR using a whole blood-islet model and a syngeneic murine transplantation model. Indeed, Del-1 pre-treatment of blood before addition of islets diminished coagulation activation and islet damage as assessed by C-peptide release. Consistently, intraportal islet-Tx in transgenic mice with endothelial cell-specific overexpression of Del-1 resulted in a marked decrease of monocytes and platelet-monocyte aggregates in the transplanted tissues, relative to those in wild-type recipients. Mechanistically, Del-1 decreased platelet-monocyte aggregate formation, by specifically blocking the interaction between monocyte Mac-1-integrin and platelet GPIb. Our findings reveal a hitherto unknown role of Del-1 in the regulation of platelet-monocyte interplay and the subsequent heterotypic aggregate formation in the context of IBMIR. Therefore, Del-1 may represent a novel approach to prevent or mitigate the adverse reactions mediated through thrombo-inflammatory pathways in islet-Tx and perhaps other inflammatory disorders involving platelet-leukocyte aggregate formation.

Indexed as

Islets of Langerhans TransplantationAnimalsBlood CoagulationBlood PlateletsCalcium-Binding ProteinsCarrier ProteinsCell Adhesion MoleculesCells, CulturedHumansInflammationIslets of LangerhansMacrophage-1 AntigenMaleMiceMice, Inbred C57BLMice, Transgenicadhesion receptorCalcium-Binding ProteinsCarrier ProteinsCell Adhesion MoleculesEDIL3 protein, humanMacrophage-1 AntigenPlatelet Glycoprotein GPIb-IX ComplexcoagulationDevelopmental endothelial locus 1 (Del-1)GPIbInstant blood-mediated inflammatory reaction (IBMIR)islet transplantationMac-1 integrinplatelet-monocyte aggregates

Identifiers

PMID26676803
PMCPMC4818166
OpenAlexW2217818916

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.