| Cytosine arabinoside induces programmed endothelial cell death through the caspase-3 pathway. | |
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MedLine Citation:
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PMID: 16581899 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The anti-cancer effects of cytosine arabinoside (ARA-C) are well known. However, effects on nonmalignant cells have not been elucidated and may be important to understanding treatment-related toxicity. The purpose of this study was to examine the effect of ARA-C on nondividing vascular endothelial cells. The objectives were to determine the effects of ARA-C on cell viability and to ascertain whether ARA-C caused apoptosis in cultured vascular endothelial cells and hydrocortisone blunted caspase-3-induced apoptosis. Endothelial cells were cultured until confluent and mitotically quiescent then exposed to ARA-C (10(-7)to 10(-3) M) for 1 to 4 days. Some experiments involved cotreatment with hydrocortisone (10(-11),10(-10),10(-4), and 10(-3) M). Light microscopy and the colorimetric MTS assay were used to measure viability. Fluorescent annexin-V and DNA fragmentation assays were used to measure apoptosis, and a fluorescence-based enzymatic assay was used to measure caspase-3 activity, which is one pathway involved in the apoptosis cascade. Two-way ANOVA or the appropriate nonparametric test was used to determine statistical significance in studies of viability and apoptosis. Oneway ANOVA was used to determine statistical significance for caspase-3 activity. Viability was decreased with higher concentrations of ARA-C and increased days of treatment. The percentage of apoptotic cells increased with higher concentrations of ARA-C and increased days of treatment. ARA-C-treated samples showed DNA fragmentation, indicative of apoptosis. Caspase-3 activity increased after ARA-C addition; hydrocortisone blunted this increase. ARA-C caused apoptosis in nondividing endothelial cells in culture. Hydrocortisone may protect against ARA-C-induced apoptosis by reducing caspase-3 activity. |
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Authors:
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Ida M Ki Moore; Carrie J Merkle; Petra Miketova; Renee K Salyer; Bonny J Torres; Richard C Schaeffer; David W Montgomery |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Biological research for nursing Volume: 7 ISSN: 1099-8004 ISO Abbreviation: Biol Res Nurs Publication Date: 2006 Apr |
Date Detail:
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Created Date: 2006-04-03 Completed Date: 2006-05-11 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9815758 Medline TA: Biol Res Nurs Country: United States |
Other Details:
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Languages: eng Pagination: 289-96 Citation Subset: IM; N |
Affiliation:
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College of Nursing, University of Arizona, Tucson 85721-0203, USA. kmoore@nursing.arizona.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Animals Anti-Inflammatory Agents / pharmacology Antimetabolites, Antineoplastic / adverse effects* Apoptosis / drug effects*, physiology Caspase 3 Caspases / drug effects*, physiology Cattle Cell Survival / drug effects Cells, Cultured Cognition Disorders / chemically induced Colorimetry Cytarabine / adverse effects* DNA Fragmentation Dose-Response Relationship, Drug Drug Evaluation, Preclinical Endothelium, Vascular* / cytology, drug effects Humans Hydrocortisone / pharmacology Microscopy, Fluorescence Microscopy, Polarization Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy Statistics, Nonparametric |
| Grant Support | |
ID/Acronym/Agency:
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NR004343/NR/NINR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Antimetabolites, Antineoplastic; 147-94-4/Cytarabine; 50-23-7/Hydrocortisone; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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