Evidence map›Paper›PMID 27629560›Full record

ArticleAutophagy2016

PRNP/prion protein regulates the secretion of exosomes modulating CAV1/caveolin-1-suppressed autophagy.

Marcos V S Dias, Bianca L Teixeira, Bruna R Rodrigues, Rita Sinigaglia-Coimbra, Isabel Porto-Carreiro, Martín Roffé, Glaucia N M Hajj, Vilma R Martins

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Integrated multi-omics elucidatesFrontiers in immunology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Post-translational modifications in prion diseases.Frontiers in molecular neuroscience · 2024
    Review
  9. Excess PrPNature communications · 2023
    Article
  10. Review
  11. Article
  12. The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022
    Review
  13. Pathogenic Extracellular Vesicle (EV) Signaling in Amyotrophic Lateral Sclerosis (ALS).Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  14. Review
  15. Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. The Role of Viral Proteins in the Regulation of Exosomes Biogenesis.Frontiers in cellular and infection microbiology · 2021
    Review
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 3 institutions in 1 country.

Marcos V S Diasa International Research Center , A.C. Camargo Cancer Center , São Paulo , Brazil , National Institute for Oncogenomics, INCITO.
Bianca L Teixeiraa International Research Center , A.C. Camargo Cancer Center , São Paulo , Brazil , National Institute for Oncogenomics, INCITO.
Bruna R Rodriguesa International Research Center , A.C. Camargo Cancer Center , São Paulo , Brazil , National Institute for Oncogenomics, INCITO.
Rita Sinigaglia-Coimbrab Electron Microscopy Center , Federal University of São Paulo , São Paulo , Brazil.
Isabel Porto-Carreiroc Paulo Niemeyer State Brain Institute , Rio de Janeiro , Brazil.
Martín Rofféa International Research Center , A.C. Camargo Cancer Center , São Paulo , Brazil , National Institute for Oncogenomics, INCITO.
Glaucia N M Hajja International Research Center , A.C. Camargo Cancer Center , São Paulo , Brazil , National Institute for Oncogenomics, INCITO.
Vilma R Martinsa International Research Center , A.C. Camargo Cancer Center , São Paulo , Brazil , National Institute for Oncogenomics, INCITO.
AC Camargo Hospital · BRInstituto Estadual do Cérebro Paulo Niemeyer · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prion protein modulates many cellular functions including the secretion of trophic factors by astrocytes. Some of these factors are found in exosomes, which are formed within multivesicular bodies (MVBs) and secreted into the extracellular space to modulate cell-cell communication. The mechanisms underlying exosome biogenesis were not completely deciphered. Here, we demonstrate that primary cultures of astrocytes and fibroblasts from prnp-null mice secreted lower levels of exosomes than wild-type cells. Furthermore, prnp-null astrocytes exhibited reduced MVB formation and increased autophagosome formation. The reconstitution of PRNP expression at the cell membrane restored exosome secretion in PRNP-deficient astrocytes, whereas macroautophagy/autophagy inhibition via BECN1 depletion reestablished exosome release in these cells. Moreover, the PRNP octapeptide repeat domain was necessary to promote exosome secretion and to impair the formation of the CAV1-dependent ATG12-ATG5 cytoplasmic complex that drives autophagosome formation. Accordingly, higher levels of CAV1 were found in lipid raft domains instead of in the cytoplasm in prnp-null cells. Collectively, these findings demonstrate that PRNP supports CAV1-suppressed autophagy to protect MVBs from sequestration into phagophores, thus facilitating exosome secretion.

Indexed as

AutophagyAnimalsAstrocytesCaveolin 1ExosomesLysosomesMembrane MicrodomainsMice, Inbred C57BLModels, BiologicalMultivesicular BodiesPrion ProteinsProtein DomainsRepetitive Sequences, Nucleic AcidStructure-Activity RelationshipCaveolin 1Prion Proteinsautophagycaveolin-1exosomesmultivesicular bodiesprion protein

Identifiers

PMID27629560
PMCPMC5103360
OpenAlexW2521023278

What OpenQuestion holds

Textmetadata
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.