Evidence map›Paper›PMID 23439251›Full record

ArticleAutophagy2013

A chimerical phagocytosis model reveals the recruitment by Sertoli cells of autophagy for the degradation of ingested illegitimate substrates.

Marina G Yefimova, Nadia Messaddeq, Thomas Harnois, Annie-Claire Meunier, Jonathan Clarhaut, Anaïs Noblanc, Jean-Luc Weickert, Anne Cantereau, Michel Philippe, Nicolas Bourmeyster and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Autophagy: A Double-Edged Sword in Male Reproduction.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. RhoG-ELMO1-RAC1 is involved in phagocytosis suppressed by mono-butyl phthalate in TM4 cells.Environmental science and pollution research international · 2018
    Article
  20. 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 5 institutions in 2 countries.

Marina G YefimovaInstitut de Physiologie et Biologie Cellulaires, CNRS-FRE 3511, Université de Poitiers, Poitiers, France.
Nadia Messaddeq
Thomas Harnois
Annie-Claire Meunier
Jonathan Clarhaut
Anaïs Noblanc
Jean-Luc Weickert
Anne Cantereau
Michel Philippe
Nicolas Bourmeyster
Omar Benzakour
Centre National de la Recherche Scientifique · FRUniversité de Poitiers · FRInserm · FRInstitut de génétique et de biologie moléculaire et cellulaire · FRInstitute of Evolutionary Physiology and Biochemistry · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phagocytosis and autophagy are typically dedicated to degradation of substrates of extrinsic and intrinsic origins respectively. Although overlaps between phagocytosis and autophagy were reported, the use of autophagy for ingested substrate degradation by nonprofessional phagocytes has not been described. Blood-separated tissues use their tissue-specific nonprofessional phagocytes for homeostatic phagocytosis. In the testis, Sertoli cells phagocytose spermatid residual bodies produced during germ cell differentiation. In the retina, pigmented epithelium phagocytoses shed photoreceptor tips produced during photoreceptor renewal. Spermatid residual bodies and shed photoreceptor tips are phosphatidylserine-exposing substrates. Activation of the tyrosine kinase receptor MERTK, which is implicated in phagocytosis of phosphatidylserine-exposing substrates, is a common feature of Sertoli and retinal pigmented epithelial cell phagocytosis. The major aim of our study was to investigate to what extent phagocytosis by Sertoli cells may be tissue specific. We analyzed in Sertoli cell cultures that were exposed to either spermatid residual bodies (legitimate substrates) or retina photoreceptor outer segments (illegitimate substrates) the course of the main phagocytosis stages. We show that whereas substrate binding and ingestion stages occur similarly for legitimate or illegitimate substrates, the degradation of illegitimate but not of legitimate substrates triggers autophagy as evidenced by the formation of double-membrane wrapping, MAP1LC3A-II/LC3-II clustering, SQSTM1/p62 degradation, and by marked changes in ATG5, ATG9 and BECN1/Beclin 1 protein expression profiles. The recruitment by nonprofessional phagocytes of autophagy for the degradation of ingested cell-derived substrates is a novel feature that may be of major importance for fundamentals of both apoptotic substrate clearance and tissue homeostasis.

Indexed as

AutophagyModels, BiologicalPhagocytosisAnimalsAutophagy-Related Protein 5c-Mer Tyrosine KinaseHumansMacrolidesMaleMicrotubule-Associated ProteinsMyosin Type IIPhosphorylationProteinsProto-Oncogene ProteinsPseudopodiaRatsAtg5 protein, ratAutophagy-Related Protein 5bafilomycin A1c-Mer Tyrosine KinaseMacrolidesMertk protein, ratMicrotubule-Associated ProteinsMyosin Type IIProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine Kinasesapoptotic substratesautophagyhomeostatic phagocytosisMERTK tyrosine kinaseprotein SSertoli cellsvitamin K-dependent factor

Identifiers

PMID23439251
PMCPMC3669177
OpenAlexW2070233181

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.