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Blood, Vol. 95 No. 3 (February 1), 2000:
pp. 846-854
Opposing effects of engagement of integrins and stimulation of
cytokine receptors on cell cycle progression of normal human
hematopoietic progenitors
Yuehua Jiang,
Felipe Prosper, and
Catherine M. Verfaillie
From the Stem Cell Laboratory and Division of Hematology, Oncology
and Transplantation, Department of Medicine and Cancer Center,
University of Minnesota, Minneapolis, MN, and the Department of
Hematology and Medical Oncology, Hospital Clinico Universitario,
University of Valencia, Valencia, Spain.
We evaluated the effect of  1-integrin receptor engagement on the
expression and activity of cell cycle regulatory proteins in
CD34+ cells under conditions that mimic the steady-state
marrow microenvironment and in the presence of supraphysiological
concentrations of interleukin-3 (IL3) and stem cell factor (SCF).
Adhesion of CD34+ progenitors to fibronectin (FN) was
similar whether IL3 or SCF was present or absent. Engagement of
1-integrins blocked S-phase entry of CD34+ cells in
the absence of IL3 or SCF, whereas addition of 10 ng/mL IL3 or SCF
prevented such a block in S-phase entry. In the absence of IL3 or SCF,
cyclin-E levels were significantly lower and p27KIP1 levels
significantly higher in FN-adherent than in FN-nonadherent cells, or
than in poly-L-lysine (PLL)-adherent or (PLL)-nonadherent cells.
Cyclin-dependent-kinase (cdk)-2 activity was decreased and levels of
cyclin-E-cdk2 complexes were lower in FN-adherent than in PLL-adherent
cells. In contrast, cyclin-E and p27KIP1 protein levels and
cdk2 activity in cells adherent to FN in the presence of IL3 or SCF
were similar to those in PLL-adherent and FN-nonadherent or
PLL-nonadherent cells. In conclusion, under physiological cytokine
conditions, integrin engagement prevents S-phase entrance of
CD34+ cells, which is associated with elevated levels of
the contact-dependent cyclin kinase inhibitor p27KIP1.
Supraphysiological concentrations of IL3 or SCF prevent
p27KIP1 elevation and override the integrin-mediated
inhibition of entry into S phase.
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