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Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents
Murine bone marrow-derived cells, dependent on interleukin 3 (IL-3) for their growth in culture, undergo programmed cell, or apoptosis, upon cytokine withdrawal. Here it is reported that a variety of DNA damaging agents cause a more rapid onset of apoptosis in a factor-dependent cell line, BAF3, dep...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1992
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119402/ https://www.ncbi.nlm.nih.gov/pubmed/1402650 |
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collection | PubMed |
description | Murine bone marrow-derived cells, dependent on interleukin 3 (IL-3) for their growth in culture, undergo programmed cell, or apoptosis, upon cytokine withdrawal. Here it is reported that a variety of DNA damaging agents cause a more rapid onset of apoptosis in a factor-dependent cell line, BAF3, deprived of IL-3. In contrast, when cultured in the presence of IL-3, or other growth promoting factors, BAF3 cells are highly resistant to X-irradiation and the cytotoxic drugs etoposide and cisplatin. Overexpression of the bcl2 gene product also protects BAF3 cells from DNA damage. The presence of IL-3 is not required during the initial events of DNA damage or its repair. In the absence of IL-3, cells still complete the repair of DNA breaks within 15 min, and continue to cycle for 5 h. At this time, IL-3 is necessary to prevent the accelerated onset of DNA cleavage from a G2 arrest point. |
format | Text |
id | pubmed-2119402 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1992 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21194022008-04-16 Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents J Exp Med Articles Murine bone marrow-derived cells, dependent on interleukin 3 (IL-3) for their growth in culture, undergo programmed cell, or apoptosis, upon cytokine withdrawal. Here it is reported that a variety of DNA damaging agents cause a more rapid onset of apoptosis in a factor-dependent cell line, BAF3, deprived of IL-3. In contrast, when cultured in the presence of IL-3, or other growth promoting factors, BAF3 cells are highly resistant to X-irradiation and the cytotoxic drugs etoposide and cisplatin. Overexpression of the bcl2 gene product also protects BAF3 cells from DNA damage. The presence of IL-3 is not required during the initial events of DNA damage or its repair. In the absence of IL-3, cells still complete the repair of DNA breaks within 15 min, and continue to cycle for 5 h. At this time, IL-3 is necessary to prevent the accelerated onset of DNA cleavage from a G2 arrest point. The Rockefeller University Press 1992-10-01 /pmc/articles/PMC2119402/ /pubmed/1402650 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents |
title | Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents |
title_full | Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents |
title_fullStr | Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents |
title_full_unstemmed | Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents |
title_short | Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents |
title_sort | interleukin 3 protects murine bone marrow cells from apoptosis induced by dna damaging agents |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119402/ https://www.ncbi.nlm.nih.gov/pubmed/1402650 |