Regulation of apoptosis in interleukin-3-dependent hemopoietic cells by interleukin-3 and calcium ionophores.
AUTOR(ES)
Rodriguez-Tarduchy, G
RESUMO
An immortalized interleukin-3 (IL-3)-dependent progenitor cell line, BAF-3, undergoes programmed cell death (apoptosis) when deprived of IL-3. This program is characterized by an early degradation of DNA into oligonucleosome-length fragments that precedes by several hours the loss of cell viability. In the absence of IL-3, DNA fragmentation and cell death can be prevented by the calcium ionophores A23187 (1 microM) and ionomycin (0.5 microM). This addition of calcium ionophore maintains cell viability while reversibly arresting the cell cycle. Apoptosis by growth factor deprivation is also a mechanism of cell elimination in bone marrow cells removed from the stromal micro-environment, as DNA fragmentation and cell death was shown to take place in primary cultures of IL-3-responsive bone marrow cells after IL-3 removal.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=552017Documentos Relacionados
- Mycoplasmal Infections Prevent Apoptosis and Induce Malignant Transformation of Interleukin-3-Dependent 32D Hematopoietic Cells
- Splenic accumulation of interleukin-3-dependent hematopoietic cells in Friend erythroleukemia.
- Establishment of an interleukin-5-dependent subclone from an interleukin-3-dependent murine hemopoietic progenitor cell line, LyD9, and its malignant transformation by autocrine secretion of interleukin-5.
- Ischemia induces partial loss of surface membrane polarity and accumulation of putative calcium ionophores.
- Interleukin 6 enhancement of interleukin 3-dependent proliferation of multipotential hemopoietic progenitors.
