Colony formation by bone marrow cells after incubation with neuraminidase. III. Cell surface repair, homing and growth characteristics of colony forming cells in vivo
Ploemacher, R.E.; Brons, N.H.; van Soest, P.L.
Experimental Hematology 9(2): 168-178
1981
ISSN/ISBN: 0301-472X PMID: 6113157 Document Number: 180906
Incubation of bone marrow cells (BMC) with neuraminidase (NA) reduced their ability to form colonies in the spleen of lethally irradiated mice to 25% of control-incubated BMC. Covering of the recipient's receptors for galactosyl residues by infusion of desialated erythrocyte membrane fragments (NA-Efr) fully prevented the reduction of NA-BMC colony formation. Upon retransplantation the desialated CFUS in the spleen of irradiated first recipients could be significantly rescued within 6 h posttransplantation by NA-Efr treatment of secondary recipients. Transplantation experiments, including NA-Efr infused and normal primary and secondary recipients, indicated that repair of the desialated CFUS cell surface probable occurred within 48 h. Establishment of growth curves indicated that desialation of CFUS did not alter their proliferative capacity but probable retarded the cells to proliferate in normal irradiated recipients for about 24 h. This might be the cause of the decreased CFUS content observed in the first recipients' spleen colonies. This delay in the onset of proliferation was not observed in mice with covered galactosyl receptors. The present experiments further indicate that (a) injected desialated CFUS are rapidly sequestrated in the recipient's body; (b) more desialated CFUS initially seed into the spleen than actually form colonies; (c) the spleen probably contains D-Galactose-specific receptors; (d) CFUS may largely restore their surface properties within 24 h following desialation, and (e) the organ distribution of normal CFUS is changed upon injection in NA-Efr infused recipients. Experiments with 51Cr-tagged BMC suggested that the organ distribution of BMC was similarly affected by neuraminidase treatment as that of CFUS.