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Serum suppresses myeloid progenitor apoptosis by regulating iron homeostasis
Author(s) -
Maclean Kirsteen,
Yang Hui,
Cleveland John L.
Publication year - 2001
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.1111
Subject(s) - progenitor cell , myeloid , haematopoiesis , microbiology and biotechnology , apoptosis , biology , programmed cell death , stem cell , cancer research , immunology , biochemistry
The growth and survival of committed hematopoietic progenitors is dependent upon cytokine signaling. However, serum is also required for optimal growth of these progenitors in culture ex vivo. Here we report that serum withdrawal leads to myeloid progenitor cell apoptosis. Although serum deprivation‐induced cell death has many hallmarks typical of apoptosis, these cell deaths were not inhibited by hemopoietins, survival factors such as IGF‐I, or treatment with a broad‐spectrum caspase inhibitor. Rather, apoptosis due to serum withdrawal was associated with damage to mitochondria. Surprisingly the serum factor required for myeloid cell survival was identified as iron, and loss of iron led to marked reductions in ATP production. Furthermore, supplementing serum‐deprived myeloid cells with bound or free iron promoted cell survival and prevented mitochondrial damage. Therefore, serum suppresses hematopoietic cell apoptosis by providing an obligate source of iron and iron homeostasis is critical for proper myeloid cell metabolism and survival. J. Cell. Biochem. 82: 171–186, 2001. © 2001 Wiley‐Liss, Inc.