Association of the expression of an SR-cyclophilin with myeloid cell
differentiation
SL Giardina, JD Coffman, HA Young, SJ Potter, JL Frey, JR Ortaldo and SK Anderson
Biological Carcinogenesis and Development Program, SAIC Frederick, MD
21702-1201, USA.
The role of a 150-kD SR-cyclophilin (NK-TR1) in monocyte differentiation
was investigated. Using an antipeptide monoclonal antibody, we have
detected NK-TR1 in human peripheral blood monocytes and HL-60 cells.
Unstimulated monocytes showed a low intracellular level of NK-TR1 protein
that increased over 3 days of lipopolysaccharide + interferon-gamma
treatment, consistent with the kinetics of monocyte differentiation. Normal
HL-60 cells also had a low level of NK-TR1 protein, and exposure to 1.25%
dimethyl sulfoxide (DMSO) resulted in a marked transient increase in
expression that returned to basal levels before the development of
granulocyte differentiation-associated biochemical changes. Phorbol
myristate acetate, a promoter of monocytic differentiation in HL-60 cells,
also caused a significant increase in NK-TR1 over basal levels.
Transfection of a vector expressing NK-TR1 antisense RNA into HL-60 cells
suppressed DMSO-mediated growth arrest. In addition, the development of a
more mature phenotype, as measured by expression of CD16, and the ability
to reduce nitroblue tetrazoleum dye was inhibited in transfectants when
compared with controls. These results are consistent with the hypothesis
that the NK-TR1 gene product is required for the progression towards a
mature differentiated phenotype.
Volume 87,
Issue 6,
pp. 2269-2274,
03/15/1996
Copyright © 1996 by The American Society of Hematology
