Evidence map›Paper›PMID 20716116›Full record

ArticleJournal of cellular and molecular medicine2011

Role of guanylate binding protein-1 in vascular defects associated with chronic inflammatory diseases.

Matthias Hammon, Martin Herrmann, Oliver Bleiziffer, Galyna Pryymachuk, Laura Andreoli, Luis E Munoz, Kerstin U Amann, Michele Mondini, Marisa Gariglio, Paolo Airó and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-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

17 citing papers in PubMed, 34 citations in OpenAlex.

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  12. Immune quiescence of the brain is set by astroglial connexin 43.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
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  16. [Pathogenesis, classification and diagnosis of necrotizing soft tissue infections].Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen · 2012
    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

16 authors at 3 institutions in 3 countries.

Matthias HammonDepartment of Plastic and Hand Surgery, University Medical Center Erlangen, Schwabachanlage 10, Erlangen, Germany.
Martin Herrmann
Oliver Bleiziffer
Galyna Pryymachuk
Laura Andreoli
Luis E Munoz
Kerstin U Amann
Michele Mondini
Marisa Gariglio
Paolo Airó
Vera S Schellerer
Antonis K Hatzopoulos
Raymund E Horch
Ulrich Kneser
Michael Stürzl
Elisabeth Naschberger
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversitätsklinikum Erlangen · DEVanderbilt University · US

Funding

Wnt-Pathway Modulators in Cardioprotection after IschemiR01HL083958 · NHLBI · VANDERBILT UNIVERSITY · PI HATZOPOULOS, ANTONIS · 2006 to 2010
$2.2M
NHLBI NIH HHS R01 HL083958
6 · The paper itself

Abstract

Rheumatic autoimmune disorders are characterized by a sustained pro-inflammatory microenvironment associated with impaired function of endothelial progenitor cells (EPC) and concomitant vascular defects. Guanylate binding protein-1 (GBP-1) is a marker and intracellular regulator of the inhibition of proliferation, migration and invasion of endothelial cells induced by several pro-inflammatory cytokines. In addition, GBP-1 is actively secreted by endothelial cells. In this study, significantly increased levels of GBP-1 were detected in the sera of patients with chronic inflammatory disorders. Accordingly we investigated the function of GBP-1 in EPC. Interestingly, stable expression of GBP-1 in T17b EPC induced premature differentiation of these cells, as indicated by a robust up-regulation of both Flk-1 and von Willebrand factor expression. In addition, GBP-1 inhibited the proliferation and migration of EPC in vitro. We confirmed that GBP-1 inhibited vessel-directed migration of EPC at the tissue level using the rat arterio-venous loop model as a novel quantitative in vivo migration assay. Overall, our findings indicate that GBP-1 contributes to vascular dysfunction in chronic inflammatory diseases by inhibiting EPC angiogenic activity via the induction of premature EPC differentiation.

Indexed as

AdultAgedAnimalsAutoimmune DiseasesCell DifferentiationCell MovementChronic DiseaseEndothelial CellsEndothelium, VascularFemaleGTP-Binding ProteinsHumansInflammationMiceMiddle AgedRatsGBP1 protein, humanGTP-Binding Proteins

Identifiers

PMID20716116
PMCPMC3823202
OpenAlexW2042365426

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.