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Regulation of hemopoietic stem cell proliferation in mice carrying the s 1j allele

, : Regulation of hemopoietic stem cell proliferation in mice carrying the s 1j allele. Cell & Tissue Kinetics 17(4): 375-386

A hemopoietic stromal defect, in mice heterozygous for the S1j allele, was investigated during hemopoietic stress induced by treatment with bacterial lipopolysaccharides (LPS) or lethal total body irradiation (TBI) and bone-marrow cell (BMC) reconstitution. Both treatments resulted in a comparable hemopoietic stem cell (CFU-s) proliferation in S1j/+ and +/+ hemopoietic organs. There was no difference in committed hemopoietic progenitor cell (BFU-e and CFU-G/M) kinetics after TBI and +/+ bone-marrow transplantation in S1j/+ and +/+ mice. The S1j/+ mice were deficient in their ability to support macroscopic spleen colony formation (65% of +/+ controls) as measured at 7 and 10 days after BMC transplantation. The S1J/+ spleen colonies contained the same number of BFU-E and CFU-G/M as colonies from +/+ spleens, while their CFU-s content was increased. On day 10 posttransplantation, the macroscopic missing colonies could be detected at the microscopic level. These small colonies contained far fewer CFU-s than the macroscopic detectable colonies. Analysis of CFU-s proliferation-inducing activities in control and post-LPS sera revealed that S1j/+ mice are normal in their ability to produce and to respond to humoral stem-cell regulators. S1j/+ mice may have a normal number of splenic stromal niches for colony formation. Of these niches, 35% are defective in its proliferative support.

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