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Mcl-1, a Bcl-2 family member, delays the death of hematopoietic cells under
a variety of apoptosis-inducing conditions
P Zhou, L Qian, KM Kozopas and RW Craig
Department of Pharmacology and Toxicology, Dartmouth Medical School,
Hanover, NH 03755-3835, USA.
Mcl-1 is a member of the Bcl-2 family that was identified based on
increased expression in myeloblastic leukemia cells undergoing
differentiation. Mcl-1 was previously found to be similar to Bcl-2 in
causing a delay in apoptotic cell death in Chinese hamster ovary cells. The
work described here was aimed at determining whether Mcl-1 could also exert
such an effect in hematopoietic cells, because endogenous Mcl-1 expression
is prominent in the hematopoietic system. A further aim was to assess the
effects of Mcl-1 in cells exposed to a variety of cytotoxic stimuli,
because Bcl-2 is known to have a broad spectrum of activity. To approach
these aims, FDC-P1 murine myeloid progenitor cells were transfected with
vectors driving either constitutive or inducible expression of Mcl-1. The
introduced Mcl-1 gene was found to cause a prolongation of viability under
various conditions that cause apoptotic cell death, including exposure to
cytotoxic agents (the chemotherapeutic drug etoposide, calcium ionophore,
or UV irradiation) and the withdrawal of required growth factors. In
addition, Mcl-1 was found to interact with Bax, a member of the Bcl-2
family that promotes cell death as a homodimer but that can heterodimerize
with Bcl-2 to promote cell viability. Although Mcl-1 prolonged cell
viability, it did not prevent eventual cell death upon continuous exposure
to a cytotoxic agent. Prolongation of viability was maximal when expression
of Mcl-1 was induced before the application of the apoptotic stimulus,
although some increase occurred if Mcl-1 was induced shortly thereafter and
before overt apoptosis. Taken as a whole, these findings provide further
parallels between Mcl-1 and Bcl-2, showing that Mcl-1 can interact with Bax
in hematopoietic FDC-P1 cells and can prolong cell viability under a
variety of cytotoxic conditions.
Volume 89,
Issue 2,
pp. 630-643,
01/15/1997
Copyright © 1997 by The American Society of Hematology
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February 1, 2002;
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J. G. Kupfner, J. J. Arcaroli, H.-K. Yum, S. G. Nadler, K.-Y. Yang, and E. Abraham
Role of NF-{kappa}B in Endotoxemia-Induced Alterations of Lung Neutrophil Apoptosis
J. Immunol.,
December 15, 2001;
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A. D. Schimmer, D. W. Hedley, L. Z. Penn, and M. D. Minden
Receptor- and mitochondrial-mediated apoptosis in acute leukemia: a translational view
Blood,
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F. Li, D. Zhang, and K. Fujise
Characterization of Fortilin, a Novel Antiapoptotic Protein
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H. Liu, H. Perlman, L. J. Pagliari, and R. M. Pope
Constitutively Activated Akt-1 Is Vital for the Survival of Human Monocyte-Differentiated Macrophages: Role of Mcl-1, Independent of Nuclear Factor (Nf)-{kappa}b, Bad, or Caspase Activation
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P. K. Epling-Burnette, B. Zhong, F. Bai, K. Jiang, R. D. Bailey, R. Garcia, R. Jove, J. Y. Djeu, T. P. Loughran Jr., and S. Wei
Cooperative Regulation of Mcl-1 by Janus Kinase/STAT and Phosphatidylinositol 3-Kinase Contribute to Granulocyte-Macrophage Colony-Stimulating Factor-Delayed Apoptosis in Human Neutrophils
J. Immunol.,
June 15, 2001;
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P. Zhou, N. B. Levy, H. Xie, L. Qian, C.-Y. G. Lee, R. D. Gascoyne, and R. W. Craig
MCL1 transgenic mice exhibit a high incidence of B-cell lymphoma manifested as a spectrum of histologic subtypes
Blood,
June 15, 2001;
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3902 - 3909.
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D. A. Moulding, R. V. Giles, D. G. Spiller, M. R. H. White, D. M. Tidd, and S. W. Edwards
Apoptosis is rapidly triggered by antisense depletion of MCL-1 in differentiating U937 cells
Blood,
September 1, 2000;
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J. L. Rinkenberger, S. Horning, B. Klocke, K. Roth, and S. J. Korsmeyer
Mcl-1 deficiency results in peri-implantation embryonic lethality
Genes & Dev.,
January 1, 2000;
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C. P. Leo, S. Y. Hsu, S.-Y. Chun, H.-W. Bae, and A. J. W. Hsueh
Characterization of the Antiapoptotic Bcl-2 Family Member Myeloid Cell Leukemia-1 (Mcl-1) and the Stimulation of Its Message by Gonadotropins in the Rat Ovary
Endocrinology,
December 1, 1999;
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J.-M. Wang, J.-R. Chao, W. Chen, M.-L. Kuo, J. J.-Y. Yen, and H.-F. Yang-Yen
The Antiapoptotic Gene mcl-1 Is Up-Regulated by the Phosphatidylinositol 3-Kinase/Akt Signaling Pathway through a Transcription Factor Complex Containing CREB
Mol. Cell. Biol.,
September 1, 1999;
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L. Klampfer, J. Cammenga, H.-G. Wisniewski, and S. D. Nimer
Sodium Salicylate Activates Caspases and Induces Apoptosis of Myeloid Leukemia Cell Lines
Blood,
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R.-m. Lee, G. Gillet, J. Burnside, S. J. Thomas, and P. Neiman
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March 15, 1999;
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K. J. Townsend, P. Zhou, L. Qian, C. K. Bieszczad, C. H. Lowrey, A. Yen, and R. W. Craig
Regulation of MCL1 through a Serum Response Factor/Elk-1-mediated Mechanism Links Expression of a Viability-promoting Member of the BCL2 Family to the Induction of Hematopoietic Cell Differentiation
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January 15, 1999;
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P. Zhou, L. Qian, C. K. Bieszczad, R. Noelle, M. Binder, N. B. Levy, and R. W. Craig
Mcl-1 in Transgenic Mice Promotes Survival in a Spectrum of Hematopoietic Cell Types and Immortalization in the Myeloid Lineage
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[Abstract]
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R. Peters, S. Leyvraz, and L. Perey
Apoptotic Regulation in Primitive Hematopoietic Precursors
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J.-R. Chao, J.-M. Wang, S.-F. Lee, H.-W. Peng, Y.-H. Lin, C.-H. Chou, J.-C. Li, H.-M. Huang, C.-K. Chou, M.-L. Kuo, et al.
mcl-1 Is an Immediate-Early Gene Activated by the Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) Signaling Pathway and Is One Component of the GM-CSF Viability Response
Mol. Cell. Biol.,
August 1, 1998;
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K. Kim, C.-k. Lee, T. J. Sayers, K. Muegge, and S. K. Durum
The Trophic Action of IL-7 on Pro-T Cells: Inhibition of Apoptosis of Pro-T1, -T2, and -T3 Cells Correlates with Bcl-2 and Bax Levels and Is Independent of Fas and p53 Pathways
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June 15, 1998;
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S. H. Kaufmann, J. E. Karp, P. A. Svingen, S. Krajewski, P. J. Burke, S. D. Gore, and J. C. Reed
Elevated Expression of the Apoptotic Regulator Mcl-1 at the Time of Leukemic Relapse
Blood,
February 1, 1998;
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A. M. Domina, J. H. Smith, and R. W. Craig
Myeloid Cell Leukemia 1 Is Phosphorylated through Two Distinct Pathways, One Associated with Extracellular Signal-regulated Kinase Activation and the Other with G2/M Accumulation or Protein Phosphatase 1/2A Inhibition
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July 7, 2000;
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C. D. Bingle, R. W. Craig, B. M. Swales, V. Singleton, P. Zhou, and M. K. B. Whyte
Exon Skipping in Mcl-1 Results in a Bcl-2 Homology Domain 3 Only Gene Product That Promotes Cell Death
J. Biol. Chem.,
July 14, 2000;
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