Vascular Endothelial Growth Factor Is Up-Regulatedin Vitroandin Vivoby Androgens

Sordello, Sylvie; Bertrand, Nicolas; Plouët, Jean

doi:10.1006/bbrc.1998.9328

Cited by 93 publications

(65 citation statements)

References 19 publications

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“…1,[19][20][21] Furthermore, the predominant angiogenic factor expressed in the normal prostate is VEGF, especially in both stromal and epithelial cells. [22][23][24] Moreover, VEGF contributes to tumor growth and progression through promotion of angiogenesis, enhancement of microvascular permeability and reduction of apoptosis. 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.…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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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“…While the VEGF promoter lacks a TATA-binding site, it contains a GC-rich core promoter region, and additional distal enhancer sites (such as, the hypoxia response elements that bind HIFl-alpha). Although hormone-responsive (7)(8)(9)(10), the VEGF promoter lacks any classical consensus androgen receptor (AR) or estrogen receptor (ER) binding sites. However, a distal ER/GC-box composite site has been identified, where ER-alpha physically interacts with the zinc finger transcription factors SP1 and SP3 to regulate VEGF levels in hormoneresponsive endometrial and breast cancer cells (10,11).…”

Section: Introductionmentioning

confidence: 99%

Regulation of vascular endothelial growth factor, VEGF, gene promoter by the tumor suppressor, WT1

Hanson

Gorman²,

Reese³

et al. 2007

Front Biosci

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Understanding angiogenesis and growth control is central for elucidating prostate tumorigenesis. However, the mechanisms of activation of the angiogenic gene, vascular endothelial growth factor (VEGF) are complex and its regulation in prostate cancer is not well understood. In previous studies, VEGF expression levels were correlated with altered levels of the zinc finger transcription factor, WTl. Since the VEGF promoter has several potential WTl binding sites and WT1 regulates many growth control genes, here we assessed whether WTl might also regulate VEGF transcription. Using transfection and DNA binding assays, functional WTl binding sites were localized within the proximal VEGF promoter. Transfection of the DDS-WTl (R394W) zinc finger mutant had no significant effect on VEGF-luciferase reporter activity, suggesting that an intact zinc finger DNA binding domain was required. Interestingly, WTl-mediated regulation of VEGF reporter constructs varied in different cell types. In androgen-responsive, LNCaP prostate cancer cells, hormone treatment enhanced WTl-mediated activation of the VEGF promoter constructs. Overall, these results suggest that WTl transcriptionally regulates VEGF through interaction of its zinc finger DNA binding domain with the proximal GC-rich VEGF promoter. These findings may shed light on the role of WTl in angiogenesis and prostate cancer progression.

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“…In the absence of these hormones by means of castration, angiogenesis is downward [7] . According to Sordello and colleagues testosterone caused an increase in transcription and biological activity of VEGF in human prostate cell culture [15] . In vivo, a transient increase in the weight of ventral lobes of the prostate gland and 7-fold increase in specific activity of VEGF belong to prostate in testosterone injected rats were seen.…”

Section: Discussionmentioning

confidence: 99%

Yaşlı Farelerin Beyninde Testosteron Takviyesinin Anjiyogenik Etkisi

Dabanoğlu¹,

Bozdoğan²,

Kum³

et al. 2017

Kafkas Univ Vet Fak Derg

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Citation of This ArticleDabanoğlu İ, Bozdoğan B, Kum Ş, Ünübol Aypak S: The angiogenic effect of testosterone supplementation on brain of aged mice. Kafkas Univ Vet Fak Derg, 23 (2): 247-251, 2017. DOI: 10.9775/kvfd.2016 AbstractThe aim of this study was to determine, by histological and molecular techniques, the effects of testosterone hormone treatment on angiogenesis in brain of aged mice. A total of 30 mice were used in 3 study groups: Sham operation group (Control), gonadectomy group (G) and gonadectomy and testosterone supplementation group (GTS). The capillary number and the inner diameter of larger capillary vessels in brain were measured by light microscope. The levels of VEGF (vascular endothelial growth factor) mRNA in brain tissues were determined by RT-PCR. After gonadectomy operation, capillary densities of brain decreased in male (P<0.05) but did not changed in female. Testosterone supplementation to gonadectomized aged mice caused a mild increase on capillary number in female brain but did not affect in male. Gonadectomy caused a decrease in VEGF mRNA levels of brain in male and female mice. Interestingly, testosterone replacement caused an important decrease (P<0.05) in the expression of VEGF of brain in male compared to control group whereas resulted with no change in female. The present results showed that testosterone hormone has different angiogenic effect on brain in male and female old mice. The gonadectomy operation in old male mice has a negative effect on angiogenic events. However, testosterone replacement in male was not sufficient to convert this change and did not increase angiogenesis.

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Vascular Endothelial Growth Factor Is Up-Regulatedin Vitroandin Vivoby Androgens

Cited by 93 publications

References 19 publications

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

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

Regulation of vascular endothelial growth factor, VEGF, gene promoter by the tumor suppressor, WT1

Yaşlı Farelerin Beyninde Testosteron Takviyesinin Anjiyogenik Etkisi

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