Stachon Axel, Aweimer Assem, Stachon Tanja, Tannapfel Andrea, Thoms Sven, Ubrig Burkhard, Köller Manfred, Krieg Michael, Truss Michael C
Institute of Clinical Chemistry, Transfusion, and Laboratory Medicine, BG-University Hospital Bergmannsheil, Ruhr-University of Bochum, Bochum, Germany.
Growth Factors. 2009 Apr;27(2):71-8. doi: 10.1080/08977190802709619.
Vascular endothelial growth factor (VEGF) is one of the most potent mitogenic factors stimulating both prostate endothelial and prostate epithelial cells. Recently, some studies reported on the endothelial secretion of a soluble VEGF receptor 2 (sVEGFR-2) that modifies the free VEGF concentration by binding VEGF. For the first time in this study, we report on the secretion and the regulation of the secretion of sVEGFR-2 by microvascular endothelial cells derived from the tissue of human benign prostatic hyperplasia (HPEC). HPEC were isolated and cultured from fresh prostate tissue. The prostate epithelial cell line BPH-1 was cultured with the supernatant of the HPEC cell culture (fractioned by fast protein liquid chromatography) and the VEGF concentration was subsequently measured. HPEC were incubated with VEGF or tumor necrosis factor alpha (TNF-alpha). Afterwards, the concentration of sVEGFR-2 in the supernatant of unstimulated and stimulated HPEC was measured by ELISA. HPEC showed a typical endothelial morphology. Under cell culture conditions sVEGFR-2 binds VEGF: The measured VEGF concentration in the supernatant of BPH-1 cells was reduced when the fractions of HPEC conditioned medium with the highest sVEGFR-2 concentration were incubated with the BPH-1 cells. The sVEGFR-2 secretion of HPEC was stimulated by VEGF and TNF-alpha. For the first time we report on the secretion of sVEGFR-2 by microvascular endothelial cells of prostate origin. The secretion of sVEGFR-2 by HPEC was stimulated by VEGF and TNF-alpha. Our data suggest that sVEGFR-2 secreted by prostate endothelial cells could modify the effect of VEGF on prostate endothelial and prostate epithelial cells.
血管内皮生长因子(VEGF)是刺激前列腺内皮细胞和前列腺上皮细胞的最有效的促有丝分裂因子之一。最近,一些研究报道了可溶性VEGF受体2(sVEGFR-2)的内皮分泌,其通过结合VEGF来改变游离VEGF的浓度。在本研究中,我们首次报道了源自人良性前列腺增生组织(HPEC)的微血管内皮细胞分泌sVEGFR-2及其分泌的调节。从新鲜前列腺组织中分离并培养HPEC。用HPEC细胞培养物的上清液(通过快速蛋白质液相色谱法分级)培养前列腺上皮细胞系BPH-1,随后测量VEGF浓度。将HPEC与VEGF或肿瘤坏死因子α(TNF-α)孵育。之后,通过ELISA测量未刺激和刺激的HPEC上清液中sVEGFR-2的浓度。HPEC呈现典型的内皮细胞形态。在细胞培养条件下,sVEGFR-2结合VEGF:当将具有最高sVEGFR-2浓度的HPEC条件培养基级分与BPH-1细胞一起孵育时,BPH-1细胞上清液中测得的VEGF浓度降低。VEGF和TNF-α刺激HPEC分泌sVEGFR-2。我们首次报道了前列腺来源的微血管内皮细胞分泌sVEGFR-2。VEGF和TNF-α刺激HPEC分泌sVEGFR-2。我们的数据表明,前列腺内皮细胞分泌的sVEGFR-2可能会改变VEGF对前列腺内皮细胞和前列腺上皮细胞的作用。