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dc.contributor.authorReipert, Siegfried
dc.contributor.authorBerry, Jeff
dc.contributor.authorHughes, Mike F
dc.contributor.authorHickman, J A
dc.contributor.authorAllen, Terence D
dc.date.accessioned2010-05-05T12:42:29Z
dc.date.available2010-05-05T12:42:29Z
dc.date.issued1995-12
dc.identifier.citationChanges of mitochondrial mass in the hemopoietic stem cell line FDCP-mix after treatment with etoposide: a correlative study by multiparameter flow cytometry and confocal and electron microscopy. 1995, 221 (2):281-8 Exp. Cell Res.en
dc.identifier.issn0014-4827
dc.identifier.pmid7493625
dc.identifier.doi10.1006/excr.1995.1376
dc.identifier.urihttp://hdl.handle.net/10541/97948
dc.description.abstractFDCP-Mix, a pluripotent murine hemopoietic stem cell line which undergoes typical internucleosomal cleavage of DNA when induced to apoptosis by either drugs or withdrawal of growth factor (interleukin-3) was studied after treatment with the topoisomerase II inhibitor etoposide (0.5-4 microM). An increase in autolytic activity was the major early morphological change within the cytoplasm, with mitochondria as the main target for autolytic digestion. Despite this macroautophagy, thin sections showed a high number of mitochondria, suggesting mitochondrial proliferation as a result of drug treatment. This observation of an increase in the number of mitochondria was confirmed by flow cytometric studies of mitochondrial overall mass. Multiparameter flow cytometry of cells double stained with propidium iodide and nonyl-acridine orange gave an accurate assay for mitochondrial mass in relation to cell cycle stages. The increase in mitochondrial mass was found in all cell cycle stages. The results suggest a drug-induced proliferation of mitochondria separate from the processes involved in the doubling of mitochondrial mass during the cell cycle and a decline of mitochondria in the later stages of apoptosis.
dc.language.isoenen
dc.subjectHaematopoietic Stem Cellsen
dc.subject.meshAcridine Orange
dc.subject.meshAnimals
dc.subject.meshApoptosis
dc.subject.meshAutolysis
dc.subject.meshCell Line
dc.subject.meshColoring Agents
dc.subject.meshCytoplasm
dc.subject.meshDNA Topoisomerases, Type II
dc.subject.meshEnzyme Inhibitors
dc.subject.meshEtoposide
dc.subject.meshFlow Cytometry
dc.subject.meshG2 Phase
dc.subject.meshHematopoietic Stem Cells
dc.subject.meshInterleukin-3
dc.subject.meshMice
dc.subject.meshMicroscopy, Confocal
dc.subject.meshMicroscopy, Electron
dc.subject.meshMitochondria
dc.subject.meshPropidium
dc.titleChanges of mitochondrial mass in the hemopoietic stem cell line FDCP-mix after treatment with etoposide: a correlative study by multiparameter flow cytometry and confocal and electron microscopy.en
dc.typeArticleen
dc.contributor.departmentDepartment of Structural Cell Biology, Paterson Institute for Cancer Research & Christie Hospital, Manchester, United Kingdom.en
dc.identifier.journalExperimental Cell Researchen
html.description.abstractFDCP-Mix, a pluripotent murine hemopoietic stem cell line which undergoes typical internucleosomal cleavage of DNA when induced to apoptosis by either drugs or withdrawal of growth factor (interleukin-3) was studied after treatment with the topoisomerase II inhibitor etoposide (0.5-4 microM). An increase in autolytic activity was the major early morphological change within the cytoplasm, with mitochondria as the main target for autolytic digestion. Despite this macroautophagy, thin sections showed a high number of mitochondria, suggesting mitochondrial proliferation as a result of drug treatment. This observation of an increase in the number of mitochondria was confirmed by flow cytometric studies of mitochondrial overall mass. Multiparameter flow cytometry of cells double stained with propidium iodide and nonyl-acridine orange gave an accurate assay for mitochondrial mass in relation to cell cycle stages. The increase in mitochondrial mass was found in all cell cycle stages. The results suggest a drug-induced proliferation of mitochondria separate from the processes involved in the doubling of mitochondrial mass during the cell cycle and a decline of mitochondria in the later stages of apoptosis.


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