Evidence map›Paper›PMID 23029139›Full record

ArticlePloS one2012

Junctional adhesion molecule (JAM)-C deficient C57BL/6 mice develop a severe hydrocephalus.

Lena Wyss, Julia Schäfer, Stefan Liebner, Michel Mittelbronn, Urban Deutsch, Gaby Enzmann, Ralf H Adams, Michel Aurrand-Lions, Karl H Plate, Beat A Imhof and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Dystonin/BPAG1 modulates diabetes and Alzheimer's disease cross-talk: a meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Pooled it
  2. Article
  3. Junctional adhesion molecule-C: A multifunctional mediator of cell adhesion.Cellular and molecular life sciences : CMLS · 2025
    Review
  4. Article
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  8. Article
  9. How Does the Immune System Enter the Brain?Frontiers in immunology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Alzheimer's disease: A matter of blood-brain barrier dysfunction?The Journal of experimental medicine · 2017
    Review
  17. Article
  18. Article
  19. Review
  20. 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

11 authors at 5 institutions in 3 countries.

Lena WyssTheodor Kocher Institute, University of Bern, Bern, Switzerland.
Julia Schäfer
Stefan Liebner
Michel Mittelbronn
Urban Deutsch
Gaby Enzmann
Ralf H Adams
Michel Aurrand-Lions
Karl H Plate
Beat A Imhof
Britta Engelhardt
University of Bern · CHGoethe University Frankfurt · DEInserm · FRUniversity of Geneva · CHUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The junctional adhesion molecule (JAM)-C is a widely expressed adhesion molecule regulating cell adhesion, cell polarity and inflammation. JAM-C expression and function in the central nervous system (CNS) has been poorly characterized to date. Here we show that JAM-C(-/-) mice backcrossed onto the C57BL/6 genetic background developed a severe hydrocephalus. An in depth immunohistochemical study revealed specific immunostaining for JAM-C in vascular endothelial cells in the CNS parenchyma, the meninges and in the choroid plexus of healthy C57BL/6 mice. Additional JAM-C immunostaining was detected on ependymal cells lining the ventricles and on choroid plexus epithelial cells. Despite the presence of hemorrhages in the brains of JAM-C(-/-) mice, our study demonstrates that development of the hydrocephalus was not due to a vascular function of JAM-C as endothelial re-expression of JAM-C failed to rescue the hydrocephalus phenotype of JAM-C(-/-) C57BL/6 mice. Evaluation of cerebrospinal fluid (CSF) circulation within the ventricular system of JAM-C(-/-) mice excluded occlusion of the cerebral aqueduct as the cause of hydrocephalus development but showed the acquisition of a block or reduction of CSF drainage from the lateral to the 3(rd) ventricle in JAM-C(-/-) C57BL/6 mice. Taken together, our study suggests that JAM-C(-/-) C57BL/6 mice model the important role for JAM-C in brain development and CSF homeostasis as recently observed in humans with a loss-of-function mutation in JAM-C.

Indexed as

AnimalsBase SequenceDNA PrimersFluorescent Antibody TechniqueHydrocephalusJunctional Adhesion Molecule CMiceMice, Inbred C57BLMice, TransgenicDNA PrimersJunctional Adhesion Molecule C

Identifiers

PMID23029139
PMCPMC3445510
OpenAlexW2029717436

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.