Ceramide Induces Release of Pro-Apoptotic Proteins from Mitochondria by Either a Ca2+-Dependent or a Ca2+-Independent Mechanism
Abstract
Several observations have been reported in the last years indicating that ceramide may activate the mitochondrial route of apoptosis. We show here that on addition of either C2- or C16-ceramide to mitochondria isolated from rat heart and suspended in a saline medium, release of cytochrome c and apoptosis-inducing factor (AIF) from the intermembrane space takes place. The release process is Ca2+ -independent and is not inhibited by Cyclosporin A (CsA). For the protein release process to occur, the presence of an oxidizable substrate is required. When mitochondria are suspended in sucrose instead of potassium medium, only short chain C2-ceramide causes cytochrome c release through a Ca2+ -dependent and CsA sensitive mitochondrial permeability transition (MPT) mechanism. The latter effect appears to be related to the membrane potential dissipating ability exhibited by short chain C2-ceramide.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Increased concentrations of ceramide may mediate apoptosis in the heart in response to ischemia or drugs or cytokines that promote apoptosis.
“Although there is much evidence that increased concentrations of ceramide may mediate apoptosis in the heart in response to ischemia or drugs or cytokines that promote apoptosis, will promote cytochrome c release and apoptosis when directly applied to cardiomyocytes, and that inhibition of de novo ceramide synthesis prevents palmitate-induced apoptosis in L6 myotubes (75, 82, 276, 355, 368), it”
From Cardiac remodeling in obesity (2008) · cites this paper as [82]
Inhibition of de novo ceramide synthesis prevents palmitate-induced apoptosis in L6 myotubes.
“Although there is much evidence that increased concentrations of ceramide may mediate apoptosis in the heart in response to ischemia or drugs or cytokines that promote apoptosis, will promote cytochrome c release and apoptosis when directly applied to cardiomyocytes, and that inhibition of de novo ceramide synthesis prevents palmitate-induced apoptosis in L6 myotubes (75, 82, 276, 355, 368), it”
From Cardiac remodeling in obesity (2008) · cites this paper as [82]
Ceramide promotes cytochrome c release and apoptosis when directly applied to cardiomyocytes.
“Although there is much evidence that increased concentrations of ceramide may mediate apoptosis in the heart in response to ischemia or drugs or cytokines that promote apoptosis, will promote cytochrome c release and apoptosis when directly applied to cardiomyocytes, and that inhibition of de novo ceramide synthesis prevents palmitate-induced apoptosis in L6 myotubes (75, 82, 276, 355, 368), it”
From Cardiac remodeling in obesity (2008) · cites this paper as [82]
The citation lists haven’t been fetched yet
References 44 · Cited by 52
- Authors
- Di Paola, M., Zaccagnino, P., Montedoro, G., Cocco, T., & Lorusso, M.
- Affiliations
- University of Bari Aldo Moro (IT)
- Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies (IT)
- Corresponding author
- Lorusso, Michele
- Venue
- Journal of Bioenergetics and Biomembranes
- Published
- 2004-04
- Volume
- 36
- Issue
- 2
- Pages
- 165-170
- ISSN
- 0145-479X (ISSN-L)
- 1573-6881
- OpenAlex
- W2065186260
- Cited by
- 52
- References
- 44
- Citations by year
- 2024: 1 · 2022: 2 · 2021: 1 · 2018: 1 · 2017: 1 · 2015: 2 · 2014: 2 · 2013: 4 · 2012: 3
- FWCI
- 2.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Journal of Bioenergetics and Biomembranes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- ceramide, mitochondrial apoptosis, cytochrome c release, apoptosis-inducing factor, mitochondrial permeability transition, cyclosporine, calcium dependence, short-chain ceramides, C2-ceramide, C16-ceramide, membrane potential, rat heart mitochondria, intermembrane space
- MeSH terms
- Animals, Apoproteins, Calcium, Cells, Cultured, Ceramides, Intracellular Membranes, Male, Membrane Potentials, Mitochondria, Heart, Osmotic Pressure, Rats, Wistar, Apoptosis, Mitochondrial Proteins, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
