Evidence map›Paper›PMID 32350079›Full record

ArticleJournal of lipid research2020

Sphingolipid distribution at mitochondria-associated membranes (MAMs) upon induction of apoptosis.

Vincent Mignard, Nolwenn Dubois, Didier Lanoé, Marie-Pierre Joalland, Lisa Oliver, Claire Pecqueur, Dominique Heymann, François Paris, François M Vallette, Lisenn Lalier

Abstract read
In one paragraph

Article in Journal of lipid research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

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  5. Low 5HTJournal of neurochemistry · 2026
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  11. Article
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  17. Article
  18. Regulation of cellular and systemic sphingolipid homeostasis.Nature reviews. Molecular cell biology · 2024
    Review
  19. Article
  20. 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

10 authors.

Vincent MignardCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France.
Nolwenn DuboisCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France.
Didier LanoéCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France.
Marie-Pierre JoallandCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France.
Lisa OliverCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; CHU de Nantes, Nantes, France.
Claire PecqueurCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France.
Dominique HeymannCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France.
François ParisCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France. Electronic address: mailto:francois.vallette@inserm.fr.
François M ValletteCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France.
Lisenn LalierCRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France; LaBCT, ICO, Saint Herblain, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The levels and composition of sphingolipids and related metabolites are altered in aging and in common disorders such as diabetes and cancers, as well as in neurodegenerative, cardiovascular, and respiratory diseases. Changes in sphingolipids have been implicated as being an essential step in mitochondria-driven cell death. However, little is known about the precise sphingolipid composition and modulation in mitochondria or related organelles. Here, we used LC-MS/MS to analyze the presence of key components of the ceramide metabolic pathway in vivo and in vitro in purified ER, mitochondria-associated membranes (MAMs), and mitochondria. Specifically, we analyzed the sphingolipids in the three pathways that generate ceramide: sphinganine in the de novo ceramide pathway, SM in the breakdown pathway, and sphingosine in the salvage pathway. We observed sphingolipid profiles in mouse liver, mouse brain, and a human glioma cell line (U251). We analyzed the quantitative and qualitative changes of these sphingolipids during staurosporine-induced apoptosis in U251 cells. Ceramide (especially C16-ceramide) levels increased during early apoptosis possibly through a conversion from mitochondrial sphinganine and SM, but sphingosine and lactosyl- and glycosyl-ceramide levels were unaffected. We also found that ceramide generation is enhanced in mitochondria when SM levels are decreased in the MAM. This decrease was associated with an increase in acid sphingomyelinase activity in MAM. We conclude that meaningful sphingolipid modifications occur in MAM, the mitochondria, and the ER during the early steps of apoptosis.

Indexed as

ApoptosisCell LineCeramidesHumansMitochondrial MembranesSphingolipidsSphingosineCeramidessafingolSphingolipidsSphingosineacid sphingomyelinaseapoptosiscell signalingceramidelipid metabolismmitochondrial outer membrane permeability

Identifiers

PMID32350079
PMCPMC7328052

What OpenQuestion holds

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Read underepoch 390

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.