Evidence map›Paper›PMID 37952151›Full record

ArticleCell reports2023

Jedi-1/MEGF12-mediated phagocytosis controls the pro-neurogenic properties of microglia in the ventricular-subventricular zone.

Vivianne Morrison, Matthew Houpert, Jonathan Trapani, Asa Brockman, Philip Kingsley, Ketaki Katdare, Hillary Layden, Gabriela Nguena-Jones, Alexandra Trevisan, Kathleen Maguire-Zeiss and 4 more

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

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Vivianne MorrisonDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA; Department of Cell and Molecular Biology, Tulane University, New Orleans, LA 70118, USA.
Matthew HoupertDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA.
Jonathan TrapaniDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA.
Asa BrockmanDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37235, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA.
Philip KingsleyDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA.
Ketaki KatdareVanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA.
Hillary LaydenDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA.
Gabriela Nguena-JonesDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA.
Alexandra TrevisanDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA; Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Kathleen Maguire-ZeissDepartment of Neuroscience, Georgetown University, Washington, DC 20057, USA.
Lawrence MarnettDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA; Department of Chemistry, Vanderbilt University, Nashville, TN 37235, USA; Department of Pharmacology, Vanderbilt University, Nashville, TN 37235, USA; A.B. Hancock Jr. Memorial Laboratory for Cancer Research, Vanderbilt-Ingram Cancer Center, Nashville, TN 37232, USA.
Gregory BixCenter for Clinical Neuroscience Research, Tulane University, New Orleans, LA 70118, USA.
Rebecca IhrieDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37235, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA.
Bruce CarterDepartment of Biochemistry, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37235, USA. Electronic address: bruce.carter@vanderbilt.edu.
Vanderbilt University · USTulane University · USGeorgetown University · USSt. Jude Children's Research Hospital · US

Funding

MULTIDISCIPLINARY TRAINING IN MOLECULAR ENDOCRINOLOGYT32DK007563 · NIDDK · VANDERBILT UNIVERSITY · PI Richard M O'Brien · 1988 to 2026
$15.9M
Overall: Eunice Kennedy Shriver Intellectual and Developmental Disabilities Research Center at VanderbiltP50HD103537 · NICHD · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Lea K Davis · 2020 to 2026
$10.3M
Training in Fundamental NeuroscienceT32MH064913 · NIMH · VANDERBILT UNIVERSITY · PI IHRIE, REBECCA A, WINDER, DANNY G. · 2001 to 2022
$7.6M
Identifying mTOR Dependent Periods During Brain DevelopmentR01NS118580 · NINDS · VANDERBILT UNIVERSITY · PI ESS, KEVIN C, IHRIE, REBECCA A · 2020 to 2024
$2.1M
PAR-1 Signaling and HANDR01NS083410 · NINDS · GEORGETOWN UNIVERSITY · PI CONANT, KATHERINE E, MAGUIRE-ZEISS, KATHLEEN ANNE · 2013 to 2017
$1.9M
The role of the glial engulfment receptor Jedi1 in regulating sensory neuron functionR01NS102365 · NINDS · VANDERBILT UNIVERSITY · PI CARTER, BRUCE D · 2018 to 2022
$1.7M
Loss of Jedi-1 impairs microglia phagocytosis, resulting in reduced postnatal neurogenesis in the ventricular-subventricular zone.F32HD107930 · NICHD · TULANE UNIVERSITY OF LOUISIANA · PI MORRISON, VIVIANNE E · 2022 to 2022
$77k
NICHD NIH HHS F32 HD107930NICHD NIH HHS P50 HD103537NIDDK NIH HHS T32 DK007563NIMH NIH HHS T32 MH064913NINDS NIH HHS R01 NS083410NINDS NIH HHS R01 NS102365NINDS NIH HHS R01 NS118580
6 · The paper itself

Abstract

Microglia are the primary phagocytes in the central nervous system and clear dead cells generated during development or disease. The phagocytic process shapes the microglia phenotype, which affects the local environment. A unique population of microglia resides in the ventricular-subventricular zone (V-SVZ) of neonatal mice, but how they influence the neurogenic niche is not well understood. Here, we demonstrate that phagocytosis contributes to a pro-neurogenic microglial phenotype in the V-SVZ and that these microglia phagocytose apoptotic cells via the engulfment receptor Jedi-1. Deletion of Jedi-1 decreases apoptotic cell clearance, triggering a neuroinflammatory microglia phenotype that resembles dysfunctional microglia in neurodegeneration and aging and that reduces neural precursor proliferation via elevated interleukin-1β signaling; interleukin-1 receptor inhibition rescues precursor proliferation in vivo. Together, these results reveal a critical role for Jedi-1 in connecting microglial phagocytic activity to the maintenance of a pro-neurogenic phenotype in the developing V-SVZ.

Indexed as

Lateral VentriclesMicrogliaAnimalsMicePhagocytesPhagocytosisReceptors, Cell SurfaceSignal TransductionPEAR1 protein, mouseReceptors, Cell SurfaceCP: Neuroscience

Identifiers

PMID37952151
PMCPMC10842823
OpenAlexW4388583222

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.