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.
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1 October 1992
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October 01 1992
Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents.
M K Collins,
M K Collins
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
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J Marvel,
J Marvel
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
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P Malde,
P Malde
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
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A Lopez-Rivas
A Lopez-Rivas
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
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M K Collins
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
J Marvel
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
P Malde
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
A Lopez-Rivas
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1992) 176 (4): 1043–1051.
Citation
M K Collins, J Marvel, P Malde, A Lopez-Rivas; Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents.. J Exp Med 1 October 1992; 176 (4): 1043–1051. doi: https://doi.org/10.1084/jem.176.4.1043
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