Proceedings of The Society for Experimental Biology and Medicine · 2000 · 14 citations · 22 references
Life SciencesEndocrinologyHematologyGene ExpressionHematopathologyStem Cell BiologyBlood Cell DifferentiationBone Marrow PhysiologyHematopoietic DevelopmentHematopoietic DifferentiationHematopoietic Stem Cell BiologyHematopoietic Stem CellsBone Marrow Erythroid ProgenitorsColony Polymerase Chain ReactionErythropoietin Receptor SignalingErythropoietin RegulationPhysiological HyperprolactinemiaProgenitor Cells
The prolactin (PRL) receptor (R), a member of the cytokine hemopoietin receptor superfamily, has been shown to activate early differentiation steps along the erythroid pathway. In particular PRL, a product of bone marrow stroma, induces functional erythropoietin (EPO)-R on CD34+ hemopoietic progenitors. In this study, expression of EPO-R mRNA and responsiveness to EPO were assessed on enriched hemopoietic progenitor cells (HPC) from seven hyperprolactinemic and three normoprolactinemic patients and two normal subjects. Expression of EPO-R mRNA by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was found in HPC of four out of seven hyperprolactinemic patients but not in normoprolactinemic patients or normal donors. Development of EPO-dependent Colony Forming Unit-Erythroid (CFU-E) colonies in semi-solid medium was observed only in hyperprolactinemic patients (six out of seven). A much higher number of CFU-E colonies was observed in the four patients with a positive EPO-R message. We conclude from these data that abnormally high levels of PRL may increase the number of EPO-responsive hemopoietic precursors in vivo as they do in vitro. Since hyperprolactinemia associates in these patients with depressed EPO production, it may be regarded as a compensatory mechanism for the reduced availability of the hemopoietic factor.
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