Evidence map›Paper›PMID 34407407›Full record

ArticleCell reports2021

The angiopoietin-Tie2 pathway regulates Purkinje cell dendritic morphogenesis in a cell-autonomous manner.

Robert Luck, Andromachi Karakatsani, Bhavin Shah, Geza Schermann, Heike Adler, Janina Kupke, Nathalie Tisch, Hyun-Woo Jeong, Michaela Kerstin Back, Florian Hetsch and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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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

19 authors at 6 institutions in 2 countries.

Robert LuckEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany.
Andromachi KarakatsaniEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany.
Bhavin ShahEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany.
Geza SchermannEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany.
Heike AdlerEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany.
Janina KupkeDepartment of Neurobiology, Interdisciplinary Centre for Neurosciences (IZN), University of Heidelberg, 69120 Heidelberg, Germany.
Nathalie TischEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany.
Hyun-Woo JeongDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, and University of Münster, Faculty of Medicine, 48149 Münster, Germany.
Michaela Kerstin BackInstitute of Pathophysiology, Focus Program Translational Neuroscience (FTN), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Florian HetschInstitute of Pathophysiology, Focus Program Translational Neuroscience (FTN), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Anna D'ErricoInstitute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, 60323 Frankfurt, Germany.
Michele De PalmaSwiss Institute for Experimental Cancer Research (ISREC), Swiss Federal Institute of Technology in Lausanne (EPFL), 1015 Lausanne, Switzerland.
Ellen WiedtkeDepartment of Infectious Diseases/Virology, Medical Faculty, University of Heidelberg, Bioquant Center, 69120 Heidelberg, Germany.
Dirk GrimmDepartment of Infectious Diseases/Virology, Medical Faculty, University of Heidelberg, Bioquant Center, 69120 Heidelberg, Germany; German Center for Infection Research (DZIF), and German Center for Cardiovascular Research (DZHK), Heidelberg, Germany.
Amparo Acker-PalmerInstitute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, 60323 Frankfurt, Germany.
Jakob von EngelhardtInstitute of Pathophysiology, Focus Program Translational Neuroscience (FTN), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Ralf H AdamsDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, and University of Münster, Faculty of Medicine, 48149 Münster, Germany.
Hellmut G AugustinEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany; Division of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), 69120 Heidelberg, Germany.
Carmen Ruiz de AlmodóvarEuropean Center of Angioscience (ECAS), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany. Electronic address: carmen.ruizdealmodovar@medma.uni-heidelberg.de.
Heidelberg University · DEJohannes Gutenberg University Mainz · DEGoethe University Frankfurt · DEUniversity of Münster · DEÉcole Polytechnique Fédérale de Lausanne · CHGerman Cancer Research Center · DE

Funding

Therapeutics Development Core (Core B)P30DK114857 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QUAGGIN, SUSAN E. · 2018 to 2022
$5.7M
NIDDK NIH HHS P30 DK114857
6 · The paper itself

Abstract

Neuro-vascular communication is essential to synchronize central nervous system development. Here, we identify angiopoietin/Tie2 as a neuro-vascular signaling axis involved in regulating dendritic morphogenesis of Purkinje cells (PCs). We show that in the developing cerebellum Tie2 expression is not restricted to blood vessels, but it is also present in PCs. Its ligands angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2) are expressed in neural cells and endothelial cells (ECs), respectively. PC-specific deletion of Tie2 results in reduced dendritic arborization, which is recapitulated in neural-specific Ang1-knockout and Ang2 full-knockout mice. Mechanistically, RNA sequencing reveals that Tie2-deficient PCs present alterations in gene expression of multiple genes involved in cytoskeleton organization, dendritic formation, growth, and branching. Functionally, mice with deletion of Tie2 in PCs present alterations in PC network functionality. Altogether, our data propose Ang/Tie2 signaling as a mediator of intercellular communication between neural cells, ECs, and PCs, required for proper PC dendritic morphogenesis and function.

Indexed as

MorphogenesisSignal TransductionAngiopoietin-1Angiopoietin-2AnimalsCerebellumDendritesGene DeletionGene Expression RegulationIntegrasesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicModels, BiologicalOrgan SpecificityAngiopoietin-1Angiopoietin-2Cre recombinaseIntegrasesReceptor, TIE-2angiogenesisangipoietinblood vesselscerebellumdendritic branchingdendritic morphologyneurodevelopmentneuro-vascularPurkinje cellTie2

Identifiers

PMID34407407
PMCPMC9110807
OpenAlexW3196210988

What Socratic 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 Socratic graph.