Primary culture of microvascular endothelial cells from human benign prostatic hyperplasia

Stachon, Axel; Schlüter, Tanja; Köller, Manfred; Weisser, Heike; Krieg, Michael

doi:10.1002/pros.1094

Cited by 10 publications

(20 citation statements)

References 32 publications

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“…TNF-a induces cell death and cell proliferation within prostate tissues. [28][29][30] In BPH, immunoreaction to TNF-a decreased as compared with that of normal prostates, while immunoreactions to both TNF receptors increased. 31 Based on the results of this study (Figures 3 and 4), we think that a low TNF-a activity in BPH is compensated by an increased amount of TNF receptors.…”

Section: Discussionmentioning

confidence: 95%

The influence of α1-antagonist on the expression pattern of TNF receptor family in primary culture of prostate epithelial cells from BPH patients

Drewa

Wolski

Misterek

et al. 2007

Prostate Cancer Prostatic Dis

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Doxazosin triggers apoptosis via an imprecisely defined receptor mechanism that is related to tumor necrosis factor receptors (TNFRs). The aim of this study was to determine CD95, TNFR-1, TNFR-2, CD40 expression in primary prostate epithelial cultures incubated with doxazosin. Epithelial cultures were cultivated from 10 benign prostate hyperplasia patients. The cells were incubated with 20, 50 and 80 lM of doxazosin. Apoptosis was confirmed by fluorescence microscopy and flow cytometry. The cells were analyzed for expression of FAS, CD40, TNFR-1 and TNFR-2 by flow cytometry. Early apoptotic cells were present in all groups. A positive correlation was noticed between doxazosin dose and TNFR-1-, -2-positive cells. A decrease of CD40-positive cell population was observed in the lowest concentration. A decrease of mean fluorescence intensity signal of CD40 and CD95 was observed in the lowest concentration. Doxazosin-triggered apoptosis was doseindependent. The initiation of apoptosis was a result of receptors 'crosstalk' rather than a single receptor pathway activation. TNF receptor self-assembly process should be checked as a potential mechanism leading to apoptosis after doxazosin treatment.

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Section: Discussionmentioning

confidence: 95%

The influence of α1-antagonist on the expression pattern of TNF receptor family in primary culture of prostate epithelial cells from BPH patients

Drewa

Wolski

Misterek

et al. 2007

Prostate Cancer Prostatic Dis

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“…The specific isolation and characterization of HPECs were extensively described before. 7 As quality control in the present study, we characterized the isolated cells by flow cytometry to ensure that HPECs are pure microvascular endothelial cells, without any significant contamination by other cell types. Therefore, we refrained from an extensive characterization to obtain satisfactory amounts of HPECs to perform our stimulation experiments.…”

Section: Discussionmentioning

confidence: 99%

“…13,25 Previously, we demonstrated the effect of VEGF on the secretion of IL-6 and endothelin-1 by HPECs, suggesting a direct regulation of the paracrine activity of HPECs by VEGF. 7,8 As a major regulator for angiogenesis, VEGF activates a plethora of signaling pathways through two tyrosine kinase receptors VEGFR-1 and VEGFR-2. 26,27 But the major signaling receptor for VEGF, mediating most of its biological activities in endothelial cells, is VEGFR-2.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] However, under physiological as well as pathological conditions, the function of microvascular endothelial cells is adapted to the respective organ and tissue. [4][5][6][7] Therefore, it is important to investigate the organ-specific function of the respective endothelium.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, the isolation and culture of microvascular endothelial cells derived from tissue of human BPH (HPECs) was reported. [7][8][9] Furthermore, for the first time we reported that HPECs secrete the soluble vascular endothelial growth factor receptor-2 (sVEGFR-2). 9 Prostatic endothelial cells secrete paracrine factors that contribute to the growth of prostate epithelial and stromal cells.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of soluble VEGFR-2 secreted by microvascular endothelial cells derived from human BPH

Aweimer

Stachon

Tannapfel

et al. 2011

Prostate Cancer Prostatic Dis

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BACKGROUND: 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. METHODS: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. RESULTS: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. CONCLUSIONS: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.

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The Secretion of Endothelin-1 by Microvascular Endothelial Cells from Human Benign Prostatic Hyperplasia is Inhibited by Vascular Endothelial Growth Factor

et al. 2004

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Prostate growth seems to be influenced by paracrine factors like endothelin-1 (ET-1), originating from the microvascular endothelium. Recently, we reported on the first isolation and primary culture of microvascular endothelial cells (HPEC) derived from tissue of human benign prostatic hyperplasia (BPH). Therefore, direct investigation of growth factor secretion by HPEC is now possible. BPH tissue was cut into small cubes and gently squeezed after incubation with dispase. HPEC were cultured from the resulting cell suspension after a stepwise selection by use of superparamagnetic beads coated with antibodies against endothelial specific antigens. HPEC were characterized by flow cytometry. After the incubation of HPEC either with vascular endothelial growth factor (VEGF), tumor necrosis factor alpha (TNF-alpha), or adenosine triphosphate (ATP), the secretion of ET-1 was measured by ELISA. HPEC showed a typical endothelial morphology. They were positive for von Willebrand factor and CD31. The ET-1 secretion of HPEC was inhibited by VEGF, but was unaffected by TNF-alpha or ATP. Furthermore, histochemistry revealed that in vivo microvascular endothelial cells were negative for ET-1. Because of the suppression by the widespread VEGF, it is unlikely that ET-1 from the microvascular endothelium acts as a growth factor in human BPH.

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Primary culture of microvascular endothelial cells from human benign prostatic hyperplasia

Abstract: For the first time, the primary culture of microvascular endothelial cells from BPH tissue was successfully performed. Our results suggest that HPEC may be actively involved in prostate growth, due to the secretion of regulatory factors such as IL-6.

Cited by 10 publications

References 32 publications

The influence of α1-antagonist on the expression pattern of TNF receptor family in primary culture of prostate epithelial cells from BPH patients

The influence of α1-antagonist on the expression pattern of TNF receptor family in primary culture of prostate epithelial cells from BPH patients

Regulation of soluble VEGFR-2 secreted by microvascular endothelial cells derived from human BPH

The Secretion of Endothelin-1 by Microvascular Endothelial Cells from Human Benign Prostatic Hyperplasia is Inhibited by Vascular Endothelial Growth Factor

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