Evidence map›Paper›PMID 24429403›Full record

ArticleKidney international2014

Lutheran/basal cell adhesion molecule accelerates progression of crescentic glomerulonephritis in mice.

Jin Huang, Anne Filipe, Cécile Rahuel, Philippe Bonnin, Laurent Mesnard, Coralie Guérin, Yu Wang, Caroline Le Van Kim, Yves Colin, Pierre-Louis Tharaux

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Kidney international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Red Blood Cell Distribution Width is Associated with Glomerulonephritis in Diabetic Patients with Albuminuria.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014
    Review
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 6 institutions in 1 country.

Jin Huang1] Paris Cardiovascular Research Centre, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [2] Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Anne Filipe1] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [2] Unité Mixte de Recherche 995, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [3] Institut National de la Transfusion Sanguine (INTS), Paris, France.
Cécile Rahuel1] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [2] Unité Mixte de Recherche 995, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [3] Institut National de la Transfusion Sanguine (INTS), Paris, France.
Philippe Bonnin1] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [2] Service d'Exploration Fonctionnelles, Hôpital Lariboisière, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France [3] Institut National de la Santé et de la Recherche Médicale (INSERM) U965, Hôpital Lariboisière, Paris, France.
Laurent Mesnard1] Unité Mixte de Recherche 702, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [2] Université Pierre et Marie Curie, Sorbonne Universités, Paris, France.
Coralie Guérin1] Paris Cardiovascular Research Centre, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [2] Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Yu Wang1] Paris Cardiovascular Research Centre, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [2] Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Caroline Le Van Kim1] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [2] Unité Mixte de Recherche 995, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [3] Institut National de la Transfusion Sanguine (INTS), Paris, France.
Yves Colin1] Université Paris Diderot, Sorbonne Paris Cité, Paris, France [2] Unité Mixte de Recherche 995, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [3] Institut National de la Transfusion Sanguine (INTS), Paris, France.
Pierre-Louis Tharaux1] Paris Cardiovascular Research Centre, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France [2] Université Paris Descartes, Sorbonne Paris Cité, Paris, France [3] Service de Néphrologie, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France.
Sorbonne Paris Cité · FRUniversité Paris Cité · FRDélégation Paris 5 · FRHôpital Lariboisière · FRInstitut National de la Transfusion Sanguine · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Migration of circulating leukocytes from the vasculature into the surrounding tissue is an important component of the inflammatory response. Among the cell surface molecules identified as contributing to leukocyte extravasation is VCAM-1, expressed on activated vascular endothelium, which participates in all stages of leukocyte-endothelial interaction by binding to leukocyte surface expressed integrin VLA-4. However, not all VLA-4-mediated events can be linked to VCAM-1. A novel interaction between VLA-4 and endothelial Lutheran (Lu) blood group antigens and basal cell adhesion molecule (BCAM) proteins has been recently shown, suggesting that Lu/BCAM may have a role in leukocyte recruitments in inflamed tissues. Here, we assessed the participation of Lu/BCAM in the immunopathogenesis of crescentic glomerulonephritis. High expression of Lu/BCAM in glomeruli of mice with rapidly progressive glomerulonephritis suggests a potential role for the local expression of Lu/BCAM in nephritogenic recruitment of leukocytes. Genetic deficiency of Lu/BCAM attenuated glomerular accumulation of T cells and macrophages, crescent formation, and proteinuria, correlating with reduced fibrin and platelet deposition in glomeruli. Furthermore, we found a pro-adhesive interaction between human monocyte α4β1 integrin and Lu/BCAM proteins. Thus, Lu/BCAM may have a critical role in facilitating the accumulation of monocytes and macrophages, thereby exacerbating renal injury.

Indexed as

Cell AdhesionAnimalsAnti-Glomerular Basement Membrane DiseaseAutoantibodiesCell Adhesion MoleculesChemotaxis, LeukocyteDisease Models, AnimalDisease ProgressionHumansIntegrin alpha4beta1KidneyLutheran Blood-Group SystemMacrophagesMaleMembrane GlycoproteinsMice, 129 Strainantiglomerular basement membrane antibodyAutoantibodiesBcam protein, mouseCell Adhesion MoleculesIntegrin alpha4beta1Lutheran Blood-Group SystemMembrane Glycoproteins

Identifiers

PMID24429403
PMCPMC4008878
OpenAlexW2074751666

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.