Evidence map›Paper›PMID 20220769›Full record

ArticleGenes and immunity2010

Quantitative lymphatic vessel trait analysis suggests Vcam1 as candidate modifier gene of inflammatory bowel disease.

G Jurisic, J P Sundberg, A Bleich, E H Leiter, K W Broman, G Buechler, L Alley, D Vestweber, M Detmar

Open access · bronzeAbstract read
In one paragraph

Article in Genes and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Mouse genome-wide association study identifies polymorphisms on chromosomes 4, 11, and 15 for age-related cardiac fibrosis.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Article
  8. Promoting inflammatory lymphangiogenesis by vascular endothelial growth factor-C (VEGF-C) aggravated intestinal inflammation in mice with experimental acute colitis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016
    Article
  9. Review
  10. Article
  11. Genetic modification of corneal neovascularization in Dstn (corn1) mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2013
    Article
  12. Article
  13. Common polymorphisms in angiogenesis.Cold Spring Harbor perspectives in medicine · 2012
    Review
  14. Article
  15. Article
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 6 institutions in 3 countries.

G JurisicInstitute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Switzerland.
J P Sundberg
A Bleich
E H Leiter
K W Broman
G Buechler
L Alley
D Vestweber
M Detmar
Jackson Laboratory · USMedizinische Hochschule Hannover · DEÉcole Polytechnique Fédérale de Lausanne · CHETH Zurich · CHMax Planck Institute for Molecular Biomedicine · DEUniversity of Wisconsin–Madison · US

Funding

TH2 CELLS DIRECT THE GENESIS OF COLONIC PATCHES AND IBDP01DK044240 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ELSON, CHARLES O · 1991 to 2003
$3.2M
VPF/VEGF IN NORMAL AND NEOPLASTIC SKIN ANGIOGENESISR01CA069184 · NCI · SWISS FEDERAL INST OF TECH (ETH ZURICH) · PI DETMAR, MICHAEL J. · 1996 to 2008
$1.6M
NCI NIH HHS CA69184NCI NIH HHS R01 CA069184NIDDK NIH HHS DK44240NIDDK NIH HHS P01 DK044240
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a chronic debilitating disease resulting from a complex interaction of multiple genetic factors with the environment. To identify modifier genes of IBD, we used an F2 intercross of IBD-resistant C57BL/6J-Il10(-/-) mice and IBD-susceptible C3H/HeJBir-Il10(-/-) (C3Bir-Il10(-/-)) mice. We found a prominent involvement of lymphatic vessels in IBD and applied a scoring system to quantify lymphatic vascular changes. Quantitative trait locus (QTL) analyses revealed a large-effect QTL on chromosome 3, mapping to an interval of 43.6 Mbp. This candidate interval was narrowed by fine mapping to 22 Mbp, and candidate genes were analyzed by a systems genetics approach that included quantitative gene expression profiling, search for functional polymorphisms, and haplotype block analysis. We identified vascular adhesion molecule 1 (Vcam1) as a candidate modifier gene in the interleukin 10-deficient mouse model of IBD. Importantly, VCAM1 protein levels were increased in susceptible C3H/HeJ mice, compared with C57BL/6J mice; systemic blockade of VCAM1 in C3Bir-Il10(-/-) mice reduced their inflammatory lymphatic vessel changes. These results indicate that genetically determined expression differences of VCAM1 are associated with susceptibility to colon inflammation, which is accompanied by extensive lymphatic vessel changes. VCAM1 is, therefore, a promising therapeutic target for IBD.

Indexed as

Genetic Predisposition to DiseaseAnimalsChromosome MappingChromosomes, MammalianFemaleGene Expression ProfilingHaplotypesInflammatory Bowel DiseasesInterleukin-10Lod ScoreLymphatic VesselsMaleMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutInterleukin-10Vascular Cell Adhesion Molecule-1

Identifiers

PMID20220769
PMCPMC2865135
OpenAlexW2076577302

What OpenQuestion holds

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Registered trials

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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.