Evidence map›Paper›PMID 36549270›Full record

ArticleNeuron2022

Endothelial PlexinD1 signaling instructs spinal cord vascularization and motor neuron development.

José Ricardo Vieira, Bhavin Shah, Sebastian Dupraz, Isidora Paredes, Patricia Himmels, Géza Schermann, Heike Adler, Alessia Motta, Lea Gärtner, Ariadna Navarro-Aragall and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  7. Molecular and Cellular Mechanisms of Motor Circuit Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Review
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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

18 authors at 8 institutions in 3 countries.

José Ricardo VieiraEuropean Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Straße 13-17, 68167 Mannheim, Germany; Faculty of Biosciences, Heidelberg University, Im Neuenheimer 234, 69120 Heidelberg, Germany.
Bhavin ShahEuropean Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Straße 13-17, 68167 Mannheim, Germany.
Sebastian DuprazInstitute for Neurovascular Cell Biology, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany.
Isidora ParedesEuropean Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Straße 13-17, 68167 Mannheim, Germany; Faculty of Biosciences, Heidelberg University, Im Neuenheimer 234, 69120 Heidelberg, Germany.
Patricia HimmelsFaculty of Biosciences, Heidelberg University, Im Neuenheimer 234, 69120 Heidelberg, Germany.
Géza SchermannEuropean Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Straße 13-17, 68167 Mannheim, Germany; Institute for Neurovascular Cell Biology, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany.
Heike AdlerEuropean Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Straße 13-17, 68167 Mannheim, Germany.
Alessia MottaSan Raffaele Scientific Institute, Division of Neuroscience, via Olgettina 60, 20132 Milan, Italy.
Lea GärtnerEuropean Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Straße 13-17, 68167 Mannheim, Germany.
Ariadna Navarro-AragallUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, EC1V 9EL London, UK.
Elena IoannouUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, EC1V 9EL London, UK.
Elena DyukovaMax-Planck-Institute for Heart and Lung Research, Ludwigstr. 43, 61231 Bad Nauheim, Germany.
Remy BonnavionMax-Planck-Institute for Heart and Lung Research, Ludwigstr. 43, 61231 Bad Nauheim, Germany.
Andreas FischerDepartment of Clinical Chemistry, University Medical Center Göttingen, Robert-Koch-Straße 40, 37075 Göttingen, Germany; Division Vascular Signaling and Cancer, German Cancer Research Center Heidelberg, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
Dario BonanomiSan Raffaele Scientific Institute, Division of Neuroscience, via Olgettina 60, 20132 Milan, Italy.
Frank BradkeLaboratory of Axon Growth and Regeneration, German Center for Neurodegenerative Diseases (DZNE), Venusberg Campus 1/99, 53127 Bonn, Germany.
Christiana RuhrbergUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, EC1V 9EL London, UK.
Carmen Ruiz de AlmodóvarEuropean Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Straße 13-17, 68167 Mannheim, Germany; Institute for Neurovascular Cell Biology, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany; Schlegel Chair for Neurovascular Cell Biology, University of Bonn, Venusberg-Campus 1, 53127 Bonn, Germany. Electronic address: carmen.ruizdealmodovar@ukbonn.de.
Heidelberg University · DEUniversity College London · GBUniversity Hospital Heidelberg · DEMax Planck Institute for Heart and Lung Research · DESan Raffaele University of Rome · ITUniversity Hospital Bonn · DEGerman Center for Neurodegenerative Diseases · DEUniversitätsmedizin Göttingen · DE

Funding

British Heart Foundation FS/19/29/34367Wellcome Trust 205099/Z/16/Z
6 · The paper itself

Abstract

How the vascular and neural compartment cooperate to achieve such a complex and highly specialized structure as the central nervous system is still unclear. Here, we reveal a crosstalk between motor neurons (MNs) and endothelial cells (ECs), necessary for the coordinated development of MNs. By analyzing cell-to-cell interaction profiles of the mouse developing spinal cord, we uncovered semaphorin 3C (Sema3C) and PlexinD1 as a communication axis between MNs and ECs. Using cell-specific knockout mice and in vitro assays, we demonstrate that removal of Sema3C in MNs, or its receptor PlexinD1 in ECs, results in premature and aberrant vascularization of MN columns. Those vascular defects impair MN axon exit from the spinal cord. Impaired PlexinD1 signaling in ECs also causes MN maturation defects at later stages. This study highlights the importance of a timely and spatially controlled communication between MNs and ECs for proper spinal cord development.

Indexed as

Endothelial CellsMotor NeuronsAnimalsAxonsMiceMice, KnockoutSignal TransductionSpinal Cordblood vesselCNS vascularizationendothelial cellmotor neuronneurodevelopmentneuro-vascular communicationPlexinD1Sema3Cspinal cord

Identifiers

PMID36549270
PMCPMC9796814
OpenAlexW4312204037

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.