| Programmed cell death (PCD). Apoptosis, autophagic PCD, or others? | |
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MedLine Citation:
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PMID: 11193023 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The occurrence of cell death as a physiological event in multicellular organisms has been known for more than 150 years; in 1972 the term apoptosis was introduced on morphological grounds. However, accumulating evidence suggests that programmed cell death (PCD) is not confined to apoptosis, but that cells use different pathways for active self-destruction as reflected by different morphology: condensation prominent, type I or apoptosis; autophagy prominent, type II; etc. Autophagic PCD appears to be a phylogenetically old phenomenon; it may occur in physiological and disease states. We have studied the relation between morphological and biochemical events during autophagic and apoptotic PCD in human mammary, lymphoblast, and colon cancer cells using electron microscopy and proteom analysis. We find that autophagic cell death (type II) PCD includes degradation of Golgi apparatus, polyribosomes, and endoplasmic reticulum, which precedes nuclear destruction. Intermediate and microfilaments are largely preserved; presumably the cytoskeleton is required for autophagocytosis. Apoptosis (type I) PCD is characterized by condensation of cytoplasm and preservation of organelles; cytoskeletal elements disintegrate in early stages. Either type of PCD involves synthesis of distinct proteins. Finally, both types of PCD share features some of a cell's stress response (e.g., translocation of hsp90). In conclusion our findings support the concept that autophagic cell death is a separate pathway of PCD distinctly different from "classical" apoptosis. However, autophagic and apoptotic PCD should not be considered as mutually exclusive phenomena. Rather, they appear to reflect a high degree of flexibility in a cell's response to changes of environmental conditions, both physiological or pathological. |
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Authors:
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W Bursch; A Ellinger; C Gerner; U Fröhwein; R Schulte-Hermann |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Annals of the New York Academy of Sciences Volume: 926 ISSN: 0077-8923 ISO Abbreviation: Ann. N. Y. Acad. Sci. Publication Date: 2000 |
Date Detail:
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Created Date: 2001-01-17 Completed Date: 2001-02-01 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7506858 Medline TA: Ann N Y Acad Sci Country: United States |
Other Details:
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Languages: eng Pagination: 1-12 Citation Subset: IM |
Affiliation:
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Institut für Krebsforschung der Universität Wien, Borschkegasse 8a, A-1090 Wien, Austria. wilfried.bursch@univie.ac.at |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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metabolism Animals Apoptosis* / drug effects, physiology Autophagy / physiology* Cytoskeleton / metabolism* Humans Keratins / metabolism Tamoxifen / pharmacology Tumor Cells, Cultured |
| Chemical | |
Reg. No./Substance:
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0/Actins; 10540-29-1/Tamoxifen; 68238-35-7/Keratins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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