ArticleThe Journal of cell biology1999
Inhibition of caspases inhibits the release of apoptotic bodies: Bcl-2 inhibits the initiation of formation of apoptotic bodies in chemotherapeutic agent-induced apoptosis.
Article in The Journal of cell biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Caulerpin Delivery via Pluronic-Free Cubosomes: Unlocking the Therapeutic Potential of a Pigment from an Invasive Marine Algae.Molecular pharmaceutics · 2025Article
- Advances in biological functions and applications of apoptotic vesicles.Cell communication and signaling : CCS · 2023Review
- New Therapeutics Targeting Arterial Media Calcification: Friend or Foe for Bone Mineralization?Metabolites · 2022Review
- Bioactive sphingolipids: Advancements and contributions from the laboratory of Dr. Lina M. Obeid.Cellular signalling · 2021Review
- Brain Ultrastructure: Putting the Pieces Together.Frontiers in cell and developmental biology · 2021Review
- Microglial and peripheral immune priming is partially sexually dimorphic in adolescent mouse offspring exposed to maternal high-fat diet.Journal of neuroinflammation · 2020Article
- StAR-related lipid transfer domain 11 (STARD11)-mediated ceramide transport mediates extracellular vesicle biogenesis.The Journal of biological chemistry · 2018Article
- Antiproliferative Activity of Crocin Involves Targeting of Microtubules in Breast Cancer Cells.Scientific reports · 2017Article
- Donor dendritic cell-derived exosomes promote allograft-targeting immune response.The Journal of clinical investigation · 2016Article
- Rho-associated coiled-coil containing kinases (ROCK): structure, regulation, and functions.Small GTPases · 2014Review
- Exosomes mediate the cell-to-cell transmission of IFN-α-induced antiviral activity.Nature immunology · 2013Article
- Time course changes of anti- and pro-apoptotic proteins in apigenin-induced genotoxicity.Chinese medicine · 2013Article
- Intracellular and Extracellular miRNAs in Regulation of Angiogenesis Signaling.Current angiogenesis · 2012Article
- Toxicity of oxidized phospholipids in cultured macrophages.Lipids in health and disease · 2012Article
- Label-free Raman observation of cytochrome c dynamics during apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Functional role of cell surface CUB domain-containing protein 1 in tumor cell dissemination.Molecular cancer research : MCR · 2009Article
- Highly twisted adamantyl arotinoids: synthesis, antiproliferative effects and RXR transactivation profiles.European journal of medicinal chemistry · 2009Article
- Measurement of cell death in mammalian cells.Current protocols in pharmacology · 2004Article
- Necrotic death of Rhodococcus equi-infected macrophages is regulated by virulence-associated plasmids.Infection and immunity · 2004Article
- Phosphate is a specific signal for ATDC5 chondrocyte maturation and apoptosis-associated mineralization: possible implication of apoptosis in the regulation of endochondral ossification.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2003Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
During apoptosis, the cell actively dismantles itself and reduces cell size by the formation and pinching off of portions of cytoplasm and nucleus as "apoptotic bodies." We have combined our previously established quantitative assay relating the amount of release of [3H]-membrane lipid to the degree of apoptosis with electron microscopy (EM) at a series of timepoints to study apoptosis of lymphoid cells exposed to vincristine or etoposide. We find that the [3H]-membrane lipid release assay correlates well with EM studies showing the formation and release of apoptotic bodies and cell death, and both processes are regulated in parallel by inducers or inhibitors of apoptosis. Overexpression of Bcl-2 or inhibition of caspases by DEVD inhibited equally well the activation of caspases as indicated by PARP cleavage. They also inhibited [3H]-membrane lipid release and release of apoptotic bodies. EM showed that cells overexpressing Bcl-2 displayed near-normal morphology and viability in response to vincristine or etoposide. In contrast, DEVD did not prevent cell death. Although DEVD inhibited the chromatin condensation, PARP cleavage, release of apoptotic bodies, and release of labeled lipid, DEVD-treated cells showed accumulation of heterogeneous vesicles trapped in the condensed cytoplasm. These results suggest that inhibition of caspases arrested the maturation and release of apoptotic bodies. Our results also imply that Bcl-2 regulates processes in addition to caspase activation.
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