Evidence map›Paper›PMID 24174685›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

CXC chemokine receptor 7 (CXCR7) affects the migration of GnRH neurons by regulating CXCL12 availability.

Fani Memi, Philipp Abe, Anna Cariboni, Fabienne MacKay, John G Parnavelas, Ralf Stumm

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

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  19. Pattern of CXCR7 Gene Expression in Mouse Brain Under Normal and Inflammatory Conditions.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
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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

6 authors at 4 institutions in 3 countries.

Fani MemiDepartment of Cell and Developmental Biology, University College London, WC1E 6BT, United Kingdom, Department of Pharmacology and Toxicology, University Hospital Jena, Friedrich-Schiller University, 07747 Jena, Germany, and Department of Immunology, Monash University, Alfred Medical Research and Education Precinct (AMREP), Melbourne, Victoria 3000, Australia.
Philipp Abe
Anna Cariboni
Fabienne MacKay
John G Parnavelas
Ralf Stumm
Jena University Hospital · DEUniversity College London · GBMonash Alfred Psychiatry Research centre · AUMRC Laboratory for Molecular Cell Biology · GB

Funding

Wellcome TrustWellcome Trust 089775
6 · The paper itself

Abstract

Gonadotropin-releasing hormone (GnRH) neurons are neuroendocrine cells, located in the hypothalamus, that play an essential role in mammalian reproduction. These neurons originate in the nasal placode and migrate during embryonic development, in association with olfactory/vomeronasal nerves, first in the nose, then through the cribriform plate to enter the forebrain, before settling in the hypothalamus. One of the molecules required for their early migration in the nose is the chemokine CXCL12, which is expressed in the embryonic nasal mesenchyme in an increasing ventral to dorsal gradient, presumably guiding GnRH neurons toward the forebrain. Mice lacking CXCR4, the receptor for CXCL12, exhibit defective GnRH cell movement and a significant reduction in their number, suggesting that CXCL12/CXCR4 signaling is important in the migration and survival of these neurons. Here, we investigated the role of the more recently identified second CXCL12 receptor, CXCR7, in GnRH neuron development. We demonstrate that CXCR7 is expressed along the migratory path of GnRH neurons in the nasal cavity and, although not expressed by GnRH neurons, it affects their migration as indicated by the ectopic accumulation of these cells in the nasal compartment in CXCR7(-/-) mice. Absence of CXCR7 caused abnormal accumulation of CXCL12-RFP at CXCR4-positive sites in the nasal area of CXCL12-RFP-transgenic mice and excessive CXCL12-dependent intracellular clustering of CXCR4 in GnRH neurons, suggesting internalization. These findings imply that CXCR7 regulates CXCL12 availability by acting as a scavenger along the migratory path of GnRH neurons and, thus, influences the migration of these cells in a noncell-autonomous manner.

Indexed as

AnimalsCell MovementChemokine CXCL12FemaleGonadotropin-Releasing HormoneMaleMiceMice, Inbred C57BLMice, TransgenicNeuronsPregnancyReceptors, CXCRReceptors, CXCR4ACKR3 protein, humanChemokine CXCL12Cmkor1 protein, mouseCxcl12 protein, mouseCXCR4 protein, humanGonadotropin-Releasing HormoneReceptors, CXCRReceptors, CXCR4

Identifiers

PMID24174685
PMCPMC3812513
OpenAlexW2002113523

What OpenQuestion holds

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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.