Fig. 4.
Fig. 4. SCF potentiates the CFU-e response to prolactin in EpoR−/− and wild-type progenitors infected with either PrlR or CHI. EpoR−/− fetal liver cells or wild-type or heterozygous littermate fetal liver cells were infected with retrovirus encoding CHI or PrlR, and cultured in either the presence (▪) or absence (▧) of SCF (100 ng/mL), in methylcellulose containing 500 ng/mL ovine-prolactin and 10% PDS. Results in each experiment were expressed as percent of colonies obtained for wild-type fetal liver cells infected with CHI and cultured in the presence of prolactin and SCF. Each determination is the mean ± SD of three independent experiments. The mean colony number per fetal liver was 540 ± 220 for PrlR-infected cells and 660 ± 198 for CHI-infected cells.

SCF potentiates the CFU-e response to prolactin in EpoR−/− and wild-type progenitors infected with either PrlR or CHI. EpoR−/− fetal liver cells or wild-type or heterozygous littermate fetal liver cells were infected with retrovirus encoding CHI or PrlR, and cultured in either the presence (▪) or absence (▧) of SCF (100 ng/mL), in methylcellulose containing 500 ng/mL ovine-prolactin and 10% PDS. Results in each experiment were expressed as percent of colonies obtained for wild-type fetal liver cells infected with CHI and cultured in the presence of prolactin and SCF. Each determination is the mean ± SD of three independent experiments. The mean colony number per fetal liver was 540 ± 220 for PrlR-infected cells and 660 ± 198 for CHI-infected cells.

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