Evidence map›Paper›PMID 14660742›Full record

ArticleThe Journal of clinical investigation2003

Proinflammatory functions of vascular endothelial growth factor in alloimmunity.

Marlies E J Reinders, Masayuki Sho, Atsushi Izawa, Ping Wang, Debabrata Mukhopadhyay, Kerith E Koss, Christopher S Geehan, Andrew D Luster, Mohamed H Sayegh, David M Briscoe

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

117 citing papers in PubMed, 244 citations in OpenAlex.

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  17. Immune Dysregulation in Endometriomas: Implications for Inflammation.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Article
  20. Review

57 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

10 authors at 3 institutions in 1 country.

Marlies E J ReindersDivision of Nephrology, Department of Medicine, Children's Hospital, 300 Longwood Avenue, Boston, Massachusetts 02115, USA.
Masayuki Sho
Atsushi Izawa
Ping Wang
Debabrata Mukhopadhyay
Kerith E Koss
Christopher S Geehan
Andrew D Luster
Mohamed H Sayegh
David M Briscoe
Harvard University · USHarvard University Press · USBoston Children's Hospital · US

Funding

IP 10--ITS ROLE IN INFLAMMATION AND CANCER THERAPYR01CA069212 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LUSTER, ANDREW D · 1996 to 2014
$5.6M
ANGIOGENESIS AND CHRONIC REJECTIONR01AI046756 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI BRISCOE, DAVID M. · 2000 to 2010
$4.2M
NCI NIH HHS CA069212NCI NIH HHS R01 CA069212NIAID NIH HHS AI46756NIAID NIH HHS R01 AI046756
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF), an established angiogenesis factor, is expressed in allografts undergoing rejection, but its function in the rejection process has not been defined. Here, we initially determined that VEGF is functional in the trafficking of human T cells into skin allografts in vivo in the humanized SCID mouse. In vitro, we found that VEGF enhanced endothelial cell expression of the chemokines monocyte chemoattractant protein 1 and IL-8, and in combination with IFN-gamma synergistically induced endothelial cell production of the potent T cell chemoattractant IFN-inducible protein-10 (IP-10). Treatment of BALB/c (H-2d) recipients of fully MHC-mismatched C57BL/6 (H-2b) donor hearts with anti-VEGF markedly inhibited T cell infiltration of allografts and acute rejection. Anti-VEGF failed to inhibit T cell activation responses in vivo, but inhibited intragraft expression of several endothelial cell adhesion molecules and chemokines, including IP-10. In addition, whereas VEGF expression was increased, neovascularization was not associated with acute rejection, and treatment of allograft recipients with the angiogenesis inhibitor endostatin failed to inhibit leukocyte infiltration of the grafts. Thus, VEGF appears to be functional in acute allograft rejection via its effects on leukocyte trafficking. Together, these observations provide mechanistic insight into the proinflammatory function of VEGF in immunity.

Indexed as

AnimalsChemokine CXCL10ChemokinesChemokines, CXCEndothelial CellsGraft RejectionHeart TransplantationHumansInflammationInterferon-gammaLeukocytesMiceMice, Inbred BALB CMice, Inbred C57BLPlatelet Endothelial Cell Adhesion Molecule-1Transplantation, HomologousChemokine CXCL10ChemokinesChemokines, CXCInterferon-gammaPlatelet Endothelial Cell Adhesion Molecule-1Vascular Endothelial Growth Factor A

Identifiers

PMID14660742
PMCPMC281640
OpenAlexW2046527998

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.