Estrogen and selective estrogen receptor modulators regulate vascular endothelial growth factor and soluble vascular endothelial growth factor receptor 1 in human endometrial stromal cells  

Oleh:

Okada, Hidetaka ; Tsutsumi, Akihiro ; Imai, Miyuki

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 93 no. 08 (Jun. 2010), page 2680-2686.
Topik: Estrogen; endometrial stromal cells; selective estrogen receptor modulator; sVEGFR-1; VEGF

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2010.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective To determine whether 17ß-estradiol (E2) and selective estrogen receptor modulators can regulate vascular endothelial growth factor (VEGF) and soluble VEGF receptor 1 (sVEGFR-1) as a VEGF antagonist in human endometrial stromal cells (ESCs). Design In vitro experiment. Setting Research laboratory at Kansai Medical University. Patient(s) Sixteen patients undergoing hysterectomy for benign reasons. Intervention(s) The ESCs were cultured with E2, 4-hydroxytamoxifen (OHT), and raloxifene. Main Outcome Measure(s) The VEGF and sVEGFR-1 messenger RNA (mRNA) levels in ESCs were determined using quantitative real-time reverse transcriptase–polymerase chain reaction (RT-PCR). Free (unbound) VEGF and sVEGFR-1 protein levels from ESCs were measured using ELISA kits. Result(s) The E2 significantly induced VEGF mRNA levels, whereas E2 caused a significant decrease in sVEGFR-1 messenger RNA (mRNA) levels. The E2 or OHT significantly increased the VEGF production levels and attenuated the sVEGFR-1 production compared with control, but raloxifene had no significant effect. The decrease in levels of free VEGF was proportional to the increase in sVEGFR-1 levels in the culture media of ESCs. Conclusion(s) The E2 or OHT stimulates VEGF production and concurrently attenuates sVEGFR-1 production in ESCs. This consequential increase in VEGF:sVEGFR-1 ratio might enhance the biological effects of VEGF on the angiogenic environment in human endometrium.

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