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• W2891501890 abstract "GCSF is widely used to treat recurrent implantation failure and use is supported by a randomized trial. We previously found endometrial GCSF receptor (GCSFR) to be primarily expressed by the stromal cells and expression was reduced in women with endometriosis-associated infertility2, a disorder characterized by impaired stromal decidualization and decreased endometrial receptivity to implantation.3 The objective of this work is to evaluate the impact of GCSF treatment on endometrial stromal decidualization. Endometrium was obtained by office sampling of 3 healthy, proliferative phase volunteers and stromal cells were isolated by enzymatic digestion and unigravity sedimentation and subject to in vitro culture and 3-5 passages. Stromal cells were treated in vitro with 10 nM estradiol and 3.8 μM medroxyprogesterone acetate (EP) +/- varying concentrations of GCSF (Sigma) for varying durations in media supplemented with 1% charcoal-stripped fetal bovine serum. Concurrent solvent controls were included in all experiments. RNA was extracted using Trizol and reverse transcribed using iScript® (BioRad). Specific mRNA transcripts were quantitated using TaqMan® PCR with pre-designed primer-probe sets (ThermoFisher). Intra- and inter-experimental variability was addressed by multiple wells per condition in each experiment and repetition of each experiment at least 2 times. As expected, stromal expression of decidualization markers, IGFBP1 and prolactin, was markedly increased (6-1000 fold) by EP treatment. Addition of 10 ng/mL GCSF augmented expression of both markers in a duration-dependent fashion: GCSF treatment increased IGFBP1 expression 1.1, 3.1, and 4.4 fold over EP alone at 8, 12, and 14 days, respectively. Prolactin expression increased 1.1, 1.3, and 6.0 fold at the same time points. GCSFR expression was increased by EP and further augmented by GCSF. GCSF response was correlated with GCSFR expression and with response to EP. The highest GCSFR expression at baseline (30 fold variance seen between cells from different subjects) predicted the highest fold increases in markers of decidualization with GCSF treatment. Similar results were seen at 1ng/mL GCSF and no reproducible effect was seen at 0.1ng/mL GCSF. GCSF augmented EP stimulation of decidual marker expression in a time and dose-dependent fashion. GCSF response was correlated with expression of its primary receptor, GCSFR. These data strongly suggest a mechanism for the observed benefit of GCSF treatment in patients with recurrent implantation failure. Previously described, reduced GCSFR expression in endometriosis patients represents a possible mechanism for altered clinical response to GCSF treatment. Ongoing work evaluating the mechanisms of GCSF action is aimed at better understanding the therapeutic role of GCSF in assisted reproduction." @default.
• W2891501890 created "2018-09-27" @default.
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• W2891501890 date "2018-09-01" @default.
• W2891501890 modified "2023-09-30" @default.
• W2891501890 title "Granulocyte colony stimulating factor (GCSF) treatment augments human endometrial decidualization: mechanism of a therapeutic effect" @default.
• W2891501890 doi "https://doi.org/10.1016/j.fertnstert.2018.07.680" @default.
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