Institute of Clinical Chemistry, Transfusion, and Laboratory Medicine, University Clinic BG Bergmannsheil, BG-University Hospital Bergmannsheil, Ruhr-University of Bochum, Bochum, Germany.
Prostate Cancer Prostatic Dis. 2012 Jun;15(2):157-64. doi: 10.1038/pcan.2011.63. Epub 2011 Dec 20.
Recently, it was reported that the soluble vascular endothelial growth factor receptor-2 (sVEGFR-2) is secreted by microvascular endothelial cells from human BPH (HPECs). The purpose of this study was to investigate the modulation of sVEGFR-2 by common endothelial cell stimulators. In addition, the physiological role of sVEGFR-2 with regard to the VEGF-stimulated proliferation of HPEC was investigated.
HPECs were isolated and cultured from fresh BPH tissue. After the incubation of HPECs either with adenosine triphosphate (ATP), interleukin (IL)-6, IL-8 or IL-12, the secretion of sVEGFR-2 was measured by enzyme-linked immunosorbent assay. For measurement of HPEC proliferation influenced by sVEGFR-2, VEGF-stimulated HPEC was cultured with/without sVEGFR-2. Cell proliferation was assessed with the Alamar Blue method.
The sVEGFR-2 secretion was increased by ATP and decreased by IL-12 and IL-8, respectively. IL-6 did not show any significant effect on sVEGFR-2 secretion of HPECs. HPEC proliferation was significantly inhibited by sVEGFR-2.
In this study, our data suggest that the secretion of sVEGFR-2 by microvascular endothelial cells from prostate origin is influenced by multiple endothelial cell stimulators. Furthermore, our data suggest that sVEGFR-2 acts as an antiangiogenic factor.
最近有报道称,可溶性血管内皮生长因子受体-2(sVEGFR-2)由人前列腺增生症(HPECs)的微血管内皮细胞分泌。本研究旨在探讨常见内皮细胞刺激物对 sVEGFR-2 的调节作用。此外,还研究了 sVEGFR-2 对 HPEC 中 VEGF 刺激增殖的生理作用。
从新鲜前列腺增生症组织中分离和培养 HPECs。在将 HPECs 分别用三磷酸腺苷(ATP)、白细胞介素(IL)-6、IL-8 或 IL-12 孵育后,通过酶联免疫吸附试验测量 sVEGFR-2 的分泌。为了测量 sVEGFR-2 对 HPEC 增殖的影响,将 VEGF 刺激的 HPEC 与/或 sVEGFR-2 一起培养。通过阿尔玛蓝法评估细胞增殖。
ATP 可增加 sVEGFR-2 的分泌,而 IL-12 和 IL-8 则分别降低 sVEGFR-2 的分泌。IL-6 对 HPEC 中 sVEGFR-2 的分泌没有明显影响。sVEGFR-2 显著抑制 HPEC 的增殖。
在这项研究中,我们的数据表明,前列腺来源的微血管内皮细胞中 sVEGFR-2 的分泌受到多种内皮细胞刺激物的影响。此外,我们的数据表明 sVEGFR-2 作为一种抗血管生成因子发挥作用。