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Heparin inhibits interferon-y signaling in human endometrial stromal cells by interference with the cellular binding of interferon-y
Oleh:
Fluhr, Herbert
;
Spratte, Julia
;
Heidrich, Stephanie
;
Ehrhardt, Jens
;
Steinmuller, Frauke
;
Zygmunt, Marek
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 95 no. 04 (Mar. 2011)
,
page 1272-1277.
Topik:
ENDOMETRIAL
;
Heparin
;
low molecular weight heparin
;
IFN-?
;
STAT-1
;
IRF-1
;
Nmi
;
endometrium
Ketersediaan
Perpustakaan FK
Nomor Panggil:
F02.K.2011.03
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
Objective To examine the impact of heparins on interferon-? (IFN-?) signaling in human endometrial stromal cells (ESCs) in vitro. Design In vitro experiment. Setting Research laboratory at a medical university center. Patient(s) Premenopausal women undergoing hysterectomy for benign reasons. Intervention(s) The ESCs were isolated from hysterectomy specimens, decidualized in vitro using P and 17ß-E2, and incubated with recombinant IFN-?, unfractionated heparin, and low molecular weight heparins (LMWHs). Main Outcome Measure(s) Interferon response factor 1 (IRF-1) and N-myc interactor (Nmi) messenger RNA (mRNA) were measured using real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Phosphorylation of signal transducer and activator of transcription 1 (STAT-1) was detected by an in-cell Western assay, expression of the IFN-? receptor by flow cytometry. Cell-bound IFN-? was determined in lysates by an ELISA. Result(s) Heparin and LMWHs inhibit the IFN-?-mediated induction of IRF-1, but not Nmi in undifferentiated and decidualized ESCs. The phosphorylation of signal transducer and activator of transcription 1 STAT-1 upon IFN-? stimulation is inhibited as well. Heparin has no effect on the IFN-? receptor in ESCs, but inhibits the binding of IFN-? to the cells. Conclusion(s) Unfractionated heparin, as well as LMWHs, are able to inhibit IFN-? signaling in human ESCs and therefore might be clinically interesting agents to modulate the actions of this proinflammatory cytokine at the implantation site.
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