Evidence map›Paper›PMID 33328887›Full record

ArticleFrontiers in cellular neuroscience2020

Differential Roles of TREM2+ Microglia in Anterograde and Retrograde Axonal Injury Models.

Gemma Manich, Ariadna Regina Gómez-López, Beatriz Almolda, Nàdia Villacampa, Mireia Recasens, Kalpana Shrivastava, Berta González, Bernardo Castellano

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  3. Review
  4. Article
  5. Article
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  10. Article
  11. Frontiers in cell and developmental biology · 2021
    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

8 authors at 1 institution in 1 country.

Gemma ManichDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Ariadna Regina Gómez-LópezDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Beatriz AlmoldaDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Nàdia VillacampaDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Mireia RecasensDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Kalpana ShrivastavaDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Berta GonzálezDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Bernardo CastellanoDepartment of Cell Biology, Physiology, and Immunology, Institute of Neuroscience, Universitat Autònoma De Barcelona, Barcelona, Spain.
Universitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are the main immune cells of the central nervous system (CNS), and they are devoted to the active surveillance of the CNS during homeostasis and disease. In the last years, the microglial receptor Triggering Receptor Expressed on Myeloid cells-2 (TREM2) has been defined to mediate several microglial functions, including phagocytosis, survival, proliferation, and migration, and to be a key regulator of a new common microglial signature induced under neurodegenerative conditions and aging, also known as disease-associated microglia (DAM). Although microglial TREM2 has been mainly studied in chronic neurodegenerative diseases, few studies address its regulation and functions in acute inflammatory injuries. In this context, the present work aims to study the regulation of TREM2 and its functions after reparative axonal injuries, using two-well established animal models of anterograde and retrograde neuronal degeneration: the perforant pathway transection (PPT) and the facial nerve axotomy (FNA). Our results indicate the appearance of a subpopulation of microglia expressing TREM2 after both anterograde and retrograde axonal injury. TREM2+ microglia were not directly related to proliferation, instead, they were associated with specific recognition and/or phagocytosis of myelin and degenerating neurons, as assessed by immunohistochemistry and flow cytometry. Characterization of TREM2+ microglia showed expression of CD16/32, CD68, and occasional Galectin-3. However, specific singularities within each model were observed in P2RY12 expression, which was only downregulated after PPT, and in ApoE, where

Indexed as

APOEIL-10 (interleukin-10)IL-6 (interleukin-6)microglial clustersneuroinflammationP2RY12phagocytosisproliferation

Identifiers

PMID33328887
PMCPMC7715005
OpenAlexW3104922314

What OpenQuestion holds

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Registered trials

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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.