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Blood, 15 October 2004, Vol. 104, No. 8, pp. 2299-2306.
Prepublished online as a Blood First Edition Paper on June 24, 2004; DOI 10.1182/blood-2004-04-1605.
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Submitted April 28, 2004
Accepted May 29, 2004
PTX Sensitive Signals in Bone Marrow Homing of Fetal and Adult Hemopoietic Progenitor Cells
Halvard Bonig, Gregory V Priestley, Lina M Nilsson, Yi Jiang, and Thalia Papayannopoulou*
Dept. of Medicine, Div. of Hematology, University of Washington, Seattle, WA, USA
Dept. of Bioengineering, University of Washington, Seattle, WA, USA
* Corresponding author; email: thalp{at}u.washington.edu.
Several examples suggest a relationship between in vitro migratory capacity and bone marrow (BM) homing. Pertussis toxin (PTX) is a potent inhibitor of serpentine receptor-associated inhibitory trimeric guanidine nucleotide binding (Gi) protein signals. As such, it blocks hemopoietic progenitor cell migration in vitro, but contrary to expectation, no effects on BM homing were observed in previous studies. We therefore re-examined the effect of PTX on homing of murine BM and fetal liver (FL). We found that BM homing of PTX-incubated progenitor cells (CFU-C) from BM or FL in irradiated and non-irradiated recipients was reduced by >75%, with a concomitant increase in circulating CFU-C in peripheral blood. Additional studies confirmed the functional significance of this reduction in homing: PTX-treated cells did not provide radio-protection, and their short-term engraftment in BM and spleen was drastically reduced. Furthermore, several approaches show that cell-intrinsic rather than host-derived mechanisms are responsible for the PTX induced homing defect. In summary, we show that Gi protein signals are required for BM homing, and as such provide a new example of the association between BM homing and in vitro migration. Moreover, our data suggest that the behavior of hemopoietic progenitors in obeying Gi signaling does not diverge from that of mature leukocytes.
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