D T Vandermolen1, Y Gu. 1. Department of Obstetrics and Gynecology, Medical College of Virginia, Richmond 23298, USA.
Abstract
PROBLEM: To investigate the expression, regulation thereof, and actions of human endometrial granulocyte colony-stimulating factor (G-CSF). METHODS: Endometrial expression of messenger ribonucleic acids for G-CSF and its receptor were studied using reverse transcriptase-polymerase chain reaction. In tissue culture, endometrial G-CSF protein production, baseline and in response to interleukin-1 beta, was determined by enzyme-linked immunosorbant assay of the conditioned media. G-CSF effects on proliferation of three choriocarcinoma cell lines were determined. RESULTS: In vivo, human endometrium expressed messenger ribonucleic acids for G-CSF and its receptor throughout the menstrual cycle, and endometrium expressed G-CSF protein in vitro. Interleukin-1 beta stimulated endometrial G-CSF protein production in time and dose dependent manners. G-CSF inhibited proliferation of two choriocarcinoma cell lines. CONCLUSIONS: These results suggest that 1) G-CSF may have physiologic roles in the endometrium throughout the menstrual cycle; 2) endometrial G-CSF protein production is stimulated by interleukin-1 beta; and 3) that G-CSF may, in part, mediate local actions of interleukin-1 beta and modulate trophoblast proliferation.
PROBLEM: To investigate the expression, regulation thereof, and actions of human endometrial granulocyte colony-stimulating factor (G-CSF). METHODS: Endometrial expression of messenger ribonucleic acids for G-CSF and its receptor were studied using reverse transcriptase-polymerase chain reaction. In tissue culture, endometrial G-CSF protein production, baseline and in response to interleukin-1 beta, was determined by enzyme-linked immunosorbant assay of the conditioned media. G-CSF effects on proliferation of three choriocarcinoma cell lines were determined. RESULTS: In vivo, human endometrium expressed messenger ribonucleic acids for G-CSF and its receptor throughout the menstrual cycle, and endometrium expressed G-CSF protein in vitro. Interleukin-1 beta stimulated endometrial G-CSF protein production in time and dose dependent manners. G-CSF inhibited proliferation of two choriocarcinoma cell lines. CONCLUSIONS: These results suggest that 1) G-CSF may have physiologic roles in the endometrium throughout the menstrual cycle; 2) endometrial G-CSF protein production is stimulated by interleukin-1 beta; and 3) that G-CSF may, in part, mediate local actions of interleukin-1 beta and modulate trophoblast proliferation.