Evidence map›Paper›PMID 36307854›Full record

ArticleCell & bioscience2022

Wasteosomes (corpora amylacea) of human brain can be phagocytosed and digested by macrophages.

Marta Riba, Joan Campo-Sabariz, Iraida Tena, Laura Molina-Porcel, Teresa Ximelis, Maria Calvo, Ruth Ferrer, Raquel Martín-Venegas, Jaume Del Valle, Jordi Vilaplana and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. 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
1.8field-weighted citation impact, top 15% 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, 18 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Uncovering tau in wasteosomes (Frontiers in aging neuroscience · 2023
    Article
  11. Wasteosomes (Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

11 authors at 3 institutions in 1 country.

Marta RibaSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Joan Campo-SabarizSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Iraida TenaSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Laura Molina-PorcelAlzheimer's Disease and Other Cognitive Disorders Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Neurology Service, Hospital Clinic, Universitat de Barcelona, Barcelona, Spain.
Teresa XimelisAlzheimer's Disease and Other Cognitive Disorders Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Neurology Service, Hospital Clinic, Universitat de Barcelona, Barcelona, Spain.
Maria CalvoUnitat de Microscòpia Òptica Avançada - Campus Clínic, Facultat de Medicina, Centres Científics i Tecnològics - Universitat de Barcelona, Barcelona, Spain.
Ruth FerrerSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Raquel Martín-VenegasSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Jaume Del ValleSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Jordi Vilaplana *Secció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain. vilaplana@ub.edu.ORCID http://orcid.org/0000-0003-2113-238X
Carme Pelegrí *Secció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Universitat de Barcelona · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ESBanc de Sang i Teixits · ES

Funding

Agencia Estatal de Investigación PID2020-115475GB-I00/AEI/ 10.13039/501100011033Ministerio de Ciencia, Innovación y Universidades FPUMinisterio de Economía y Competitividad BFU2016-78398-P
6 · The paper itself

Abstract

backgroundCorpora amylacea of human brain, recently renamed as wasteosomes, are granular structures that appear during aging and also accumulate in specific areas of the brain in neurodegenerative conditions. Acting as waste containers, wasteosomes are formed by polyglucosan aggregates that entrap and isolate toxic and waste substances of different origins. They are expelled from the brain to the cerebrospinal fluid (CSF), and can be phagocytosed by macrophages. In the present study, we analyze the phagocytosis of wasteosomes and the mechanisms involved in this process. Accordingly, we purified wasteosomes from post-mortem extracted human CSF and incubated them with THP-1 macrophages. Immunofluorescence staining and time-lapse recording techniques were performed to evaluate the phagocytosis. We also immunostained human hippocampal sections to study possible interactions between wasteosomes and macrophages at central nervous system interfaces.

resultsWe observed that the wasteosomes obtained from post-mortem extracted CSF are opsonized by MBL and the C3b complement protein. Moreover, we observed that CD206 and CD35 receptors may be involved in the phagocytosis of these wasteosomes by THP-1 macrophages. Once phagocytosed, wasteosomes become degraded and some of the resulting fractions can be exposed on the surface of macrophages and interchanged between different macrophages. However, brain tissue studies show that, in physiological conditions, CD206 but not CD35 receptors may be involved in the phagocytosis of wasteosomes.

conclusionsThe present study indicates that macrophages have the machinery required to process and degrade wasteosomes, and that macrophages can interact in different ways with wasteosomes. In physiological conditions, the main mechanism involve CD206 receptors and M2 macrophages, which trigger the phagocytosis of wasteosomes without inducing inflammatory responses, thus avoiding tissue damage. However, altered wasteosomes like those obtained from post-mortem extracted CSF, which may exhibit waste elements, become opsonized by MBL and C3b, and so CD35 receptors constitute another possible mechanism of phagocytosis, leading in this case to inflammatory responses.

Indexed as

BrainC3bCD206CD35Corpora amylaceaIgMNatural immunityPhagocytosisWasteosome

Identifiers

PMID36307854
PMCPMC9617366
OpenAlexW4307714096

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.