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Blood, Vol. 95 No. 9 (May 1), 2000:
pp. 2742-2747
PLENARY PAPER
Specific and rapid induction of the proapoptotic protein Hrk
after growth factor withdrawal in hematopoietic progenitor cells
Cristina Sanz,
Adalberto Benito,
Naohiro Inohara,
Daryoush Ekhterae,
Gabriel Nunez, and
Jose Luis Fernandez-Luna
From the Servicio de Inmunologia, Hospital Universitario Marques de
Valdecilla, INSALUD, Santander, Spain, and Department of Pathology,
University of Michigan Medical School, Ann Arbor, MI.
Hrk is a newly described proapoptotic member of the Bcl-2 family
that is mainly expressed in hematopoietic tissues and cultured neurons.
In this study we have examined the expression and activity of Hrk in
hematopoietic progenitors. To address these issues, we used 3 growth
factor-dependent murine hematopoietic cell lines, HCD-57, FDCP-Mix, and
FL5.12. The expression of Hrk was undetectable in cells cultured with
growth factors, but it was rapidly up-regulated on growth factor
withdrawal. In contrast, the expression of Bcl-xL decreased
and that of proapoptotic Bax, Bad, and Bak was unchanged or
down-regulated after removal of growth factors. This pattern of
expression correlated with the induction of apoptosis. Hrk was also up-regulated in human cell lines and in bone marrow-derived CD34+ cells cultured in the absence of growth factors. In
addition, the levels of Hrk were up-regulated after treatment with the
chemotherapeutic drug etoposide. Expression of prosurvival
Bcl-xL or Bcl-2 proteins blocked the induction of Hrk. Hrk
was induced in FDCP-Mix cells treated with ionomicin in the presence of
IL-3, suggesting that cytosolic calcium may regulate the expression of
this proapoptotic protein. Furthermore, ectopic expression of Hrk
induced cell death of hematopoietic progenitors in the presence of
IL-3. Thus, Hrk is specifically and rapidly induced in hematopoietic
progenitors after growth factor deprivation or treatment with
chemotherapeutic drugs, and this may be sufficient
to induce apoptosis in these cells.
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