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Human Endometrial Expression of Granulocyte Colony‐Stimulating Factor (G‐CSF) and Its Receptor, Stimulation of Endometrial G‐CSF Production by Interleukin‐1β, and G‐CSF Inhibition of Choriocarcinoma Cell Proliferation
Author(s) -
Vandermolen David T.,
Gu Yang
Publication year - 1996
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.1996.tb00177.x
Subject(s) - stimulation , granulocyte colony stimulating factor , granulocyte colony stimulating factor receptor , choriocarcinoma , granulocyte macrophage colony stimulating factor , receptor , medicine , endocrinology , colony stimulating factor , biology , cytokine , microbiology and biotechnology , haematopoiesis , chemotherapy , stem cell
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‐1β, 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‐1β 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‐1β; and 3) that G‐CSF may, in part, mediate local actions of interleukin‐1β and modulate trophoblast proliferation.