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J. Biol. Chem., Vol. 278, Issue 11, 9235-9243, March 14, 2003

This Article Full Text Full Text (PDF) All Versions of this Article: 278/11/9235    most recent M205528200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Apáti, A. Articles by Magócsi, M. Search for Related Content PubMed PubMed Citation Articles by Apáti, A. Articles by Magócsi, M. Social Bookmarking                      What's this?

Calcium Induces Cell Survival and Proliferation through the Activation of the MAPK Pathway in a Human Hormone-dependent Leukemia Cell Line, TF-1^*

Ágota Apáti, Judit Jánossy^§, Anna Brózik, Pál Imre Bauer^¶, and Mária Magócsi

From the  Department of Cell Metabolism, National Medical Centre, Institute of Haematology and Immunology, Diószegi út 64, Budapest H-1113, the ^§ Institute of Enzymology, Hungarian Academy of Sciences, Budapest H-1113, and the ^¶ Department of Medical Biochemistry, Semmelweis University, Budapest H-1088, Hungary

Survival and proliferation of cells of a human myelo-erythroid CD34+ leukemia cell line (TF-1) depend on the presence of granulocyte-macrophage colony-stimulating factor or interleukin-3. Upon hormone withdrawal these cells stop proliferating and undergo apoptotic process. In this report 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 up-regulated. 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 and 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 with only a small increase of Egr-1 and 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.

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