Dysregulated bcl-2 expression inhibits apoptosis but not differentiation of retinoic acid-induced HL-60 granulocytes

Ulie R. Park, Kent Robertson, Dennis D. Hickstein, Schickwann Tsai, David M. Hockenbery, Steven J. Collins

Research output: Contribution to journalArticle

98 Scopus citations

Abstract

The bcl-2 proto-oncogene appears to contribute to the development of certain malignancies by inhibiting programmed cell death (apoptosis). Mature granulocytes show a markedly limited life span and rapidly undergo apoptosis. To further define the relationship between apoptosis and granulocyte differentiation, we used retroviral vector-mediated gene transduction to introduce the normal bcl-2 gene into the HL-60 myeloid leukemia cell line and determined the response of these bcl-2-transduced HL-60 cells to the induction of granulocyte differentiation by retinoic acid (RA). Although the bcl-2-transduced HL-60 cells showed the same differentiative response to RA as did the parental HL-60 cells, the life span of the RA-induced, bcl-2- transduced HL-60 granulocytes was markedly prolonged compared with that of the RA-induced parental HL-60 granulocytes. DNA fragmentation studies indicate that this prolonged life span resulted from diminished apoptosis in the bcl-2-transduced cells. These studies indicate that bcl-2 is involved in regulating apoptosis in maturing granulocytes. Because bcl-2 overexpression did not interfere with RA-induced granulocyte differentiation, it appears that granulocyte differentiation and apoptosis are under distinct and separate regulatory controls.

Original languageEnglish (US)
Pages (from-to)440-445
Number of pages6
JournalBlood
Volume84
Issue number2
DOIs
StatePublished - Jul 15 1994

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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