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Papers In Press, published online ahead of print January 6, 2003
Dept. of Cell Metabolism, Natl.Medical Center, Budapest H-1113
Corresponding Author: magocsi{at}biomembrane.hu
Survival and proliferation of cells of a human myelo-erythroid CD34+ leukaemia cell line (TF-1) depend on the presence of GM-CSF or IL-3. Upon hormone withdrawal these cells stop proliferating and undergo apoptotic process. In this paper we demonstrate that a controlled increase in [Ca2+]i induces hormone-independent survival and proliferation of TF-1 cells. We found that moderate elevation of [Ca2+]i by the addition of cyclopiasonic-acid protected TF1 cells from apoptosis. Furthermore, a higher, but transient elevation of [Ca2+]i by ionomycin treatment induced cell proliferation. In both cases caspase-3 activity was reduced, and Bcl-2 was upregulated. Higher elevation of [Ca2+]i by ionomycin induced MEK-dependent biphasic ERK1/2 activation, sufficient to move the cells from G0/G1 to S/M phases. Meanwhile activation of ERK1/2, phosphorylation of the Elk-1 transcription factor, and consequently a substantial elevation of Egr-1 and c-Fos levels, as well as AP-1 DNA binding were observed. Moderate elevation of [Ca2+]i, on the other hand, caused a delayed monophasic activation of ERK1/2 and Elk-1 that was accompanied only with a small increase of Egr-1, c-Fos levels and AP-1 DNA binding. The specific MEK-1 kinase inhibitor, PD98059, inhibited all the effects of increasing [Ca2+]i, indicating that the MAPK/ERK pathway activation is essential for TF-1 cell survival and proliferation. Based on these results we suggest that the elevation of the [Ca2+]i may influence the cytokine dependence of hemopoietic progenitors and may contribute to pathological hematopoiesis.
J. Biol. Chem, 10.1074/jbc.M205528200
Submitted on June 4, 2002
Revised on January 6, 2003
Accepted on January 6, 2003
Calcium induces cell survival and proliferation through the activation of MAPK pathway in a human hormone-dependent leukaemia cell line (TF-1)
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