scholarly journals VEGF, VEGF165b and EG-VEGF expression is specifically related with hormone profile in pituitary adenomas

2019 ◽  
Vol 63 (1) ◽  
Author(s):  
Ana Silvia Corlan ◽  
Anca Maria Cîmpean ◽  
Eugen Melnic ◽  
Marius Raica ◽  
Simona Sarb
Keyword(s):  
Pituitary Adenomas ◽  
P Value ◽  
Endocrine Gland ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Folliculostellate Cells ◽  
Hormone Profile ◽  
Hormonal Milieu ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF), its inhibitory splice variant, VEGF165b and Endocrine Gland derived VEGF (EG-VEGF) have a controversial role in pituitary gland. We aim to study VEGF, VEGF165b and EG-VEGF expression in pituitary adenomas. A significant correlation was found between growth hormone (GH) and VEGF secretion (P=0.024). For prolactinomas, VEGF and prolactin expression, had a P-value of 0.02 for Kendall coefficient and a P-value of 0.043 for the Spearman coefficient. VEGF-mRNA amplification was detected in both tumor cells and folliculostellate cells. VEGF165b was positive in 16.66% of pituitary adenomas. EG-VEGF was significantly correlated with prolactin (P=0.025) and luteinizing hormone (P=0.028). Our data strongly support VEGF, VEGF165b and EG-VEGF as important players of pituitary adenomas tumorigenesis. Particular hormonal milieu heterogeneity, special vascular network with an unusual reactivity to tumor growth correlated with variability of VEGF, VEGF165b and EG-VEGF secretion may stratify pituitary adenomas in several molecular groups with a direct impact on therapy and prognosis.

Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema

1998 ◽  
Vol 85 (1) ◽  
pp. 53-57 ◽  
Author(s):  
Fengping Xu ◽  
John W. Severinghaus
Keyword(s):  
High Altitude ◽  
Cerebral Edema ◽  
Northern Blot Analysis ◽  
Capillary Permeability ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
High Altitude Cerebral Edema ◽  
Alveolar Hypoxia ◽  
Endothelial Growth Factor

The mechanism by which hypoxia causes high-altitude cerebral edema (HACE) is unknown. Tissue hypoxia triggers angiogenesis, initially by expressing vascular endothelial growth factor (VEGF), which has been shown to increase extracerebral capillary permeability. This study investigated brain VEGF expression in 32 rats exposed to progressively severe normobaric hypoxia (9–6% O2) for 0 (control), 3, 6, or 12 h or 1, 2, 3, or 6 days. O2concentration was adjusted intermittently to the limit of tolerance by activity and intake, but no attempt was made to detect HACE. Northern blot analysis demonstrated that two molecular bands of transcribed VEGF mRNA (∼3.9 and 4.7 kb) were upregulated in cortex and cerebellum after as little as 3 h of hypoxia, with a threefold increase peaking at 12–24 h. Western blot revealed that VEGF protein was increased after 12 h of hypoxia, reaching a maximum in ∼2 days. The expression of flt-1 mRNA was enhanced after 3 days of hypoxia. We conclude that VEGF production in hypoxia is consistent with the hypothesis that angiogenesis may be involved in HACE.

Transforming growth factor-β1 modulates the expression of vascular endothelial growth factor by osteoblasts

1999 ◽  
Vol 277 (4) ◽  
pp. C628-C637 ◽  
Author(s):  
Pierre B. Saadeh ◽  
Babak J. Mehrara ◽  
Douglas S. Steinbrech ◽  
Matthew E. Dudziak ◽  
Joshua A. Greenwald ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Endothelial Growth Factor ◽  
Dose Dependent ◽  
Tgf Β1 ◽  
Vegf Protein

Angiogenesis is essential to both normal and pathological bone physiology. Vascular endothelial growth factor (VEGF) has been implicated in angiogenesis, whereas transforming growth factor-β1 (TGF-β1) modulates bone differentiation, matrix formation, and cytokine expression. The purpose of this study was to investigate the relationship between TGF-β1 and VEGF expression in osteoblasts and osteoblast-like cells. Northern blot analysis revealed an early peak of VEGF mRNA (6-fold at 3 h) in fetal rat calvarial cells and MC3T3-E1 osteoblast-like cells after stimulation with TGF-β1 (2.5 ng/ml). The stability of VEGF mRNA in MC3T3-E1 cells was not increased after TGF-β1 treatment. Actinomycin D inhibited the TGF-β1-induced peak in VEGF mRNA, whereas cycloheximide did not. Blockade of TGF-β1 signal transduction via a dominant-negative receptor II adenovirus significantly decreased TGF-β1 induction of VEGF mRNA. Additionally, TGF-β1 induced a dose-dependent increase in VEGF protein expression by MC3T3-E1 cells ( P < 0.01). Dexamethasone similarly inhibited VEGF protein expression. Both TGF-β1 mRNA and VEGF mRNA were concurrently present in rat membranous bone, and both followed similar patterns of expression during rat mandibular fracture healing (mRNA and protein). In summary, TGF-β1-induced VEGF expression by osteoblasts and osteoblast-like cells is a dose-dependent event that may be intimately related to bone development and fracture healing.

scholarly journals Hypoxic Regulation of Vascular Endothelial Growth Factor mRNA Stability Requires the Cooperation of Multiple RNA Elements

1999 ◽  
Vol 10 (4) ◽  
pp. 907-919 ◽  
Author(s):  
J. A. Dibbens ◽  
D. L. Miller ◽  
A. Damert ◽  
W. Risau ◽  
M. A. Vadas ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Coding Region ◽  
Vegf Gene ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Rapid Degradation ◽  
Multiple Regions ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a key regulator of developmental, physiological, and tumor angiogenesis. Upregulation of VEGF expression by hypoxia appears to be a critical step in the neovascularization of solid cancers. The VEGF mRNA is intrinsically labile, but in response to hypoxia the mRNA is stabilized. We have systematically analyzed the regions in the VEGF mRNA that are responsible for its lability under normoxic conditions and for stabilization in response to hypoxia. We find that the VEGF mRNA not only contains destabilizing elements in its 3′ untranslated region (3′UTR), but also contains destabilizing elements in the 5′UTR and coding region. Each region can independently promote mRNA degradation, and together they act additively to effect rapid degradation under normoxic conditions. Stabilization of the mRNA in response to hypoxia is completely dependent on the cooperation of elements in each of the 5′UTR, coding region, and 3′UTR. Combinations of any of two of these three regions were completely ineffective in responding to hypoxia, whereas combining all three regions allowed recapitulation of the hypoxic stabilization seen with the endogenous VEGF mRNA. We conclude that multiple regions in the VEGF mRNA cooperate both to ensure the rapid degradation of the mRNA under normoxic conditions and to allow stabilization of the mRNA in response to hypoxia. Our findings highlight the complexity of VEGF gene expression and also reveal a mechanism of gene regulation that could become the target for strategies of therapeutic intervention.

Vascular endothelial growth factor (VEGF) expression in human pituitary adenomas and carcinomas

1999 ◽  
Vol 10 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Ricardo V. Lloyd ◽  
Bernd W. Scheithauer ◽  
Takao Kuroki ◽  
Sergio Vidal ◽  
Kalman Kovacs ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Pituitary Adenomas ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Human Pituitary ◽  
Human Pituitary Adenomas ◽  
Endothelial Growth Factor

Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) expression in colorectal cancer

2007 ◽  
Vol 96 (7) ◽  
pp. 605-610 ◽  
Author(s):  
Hideki Nagano ◽  
Takanori Goi ◽  
Kenji Koneri ◽  
Yasuo Hirono ◽  
Kanji Katayama ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Endocrine Gland ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Endothelial Growth Factor

scholarly journals ANALYSIS OF THE INTERRELATION OF THE VASCULAR ENDOTHELIAL GROWTH FACTOR WITH PITUITARY ADENOMAS COMPLICATED BY PITUITARY APOPLEXY

2017 ◽  
Vol 22 (3) ◽  
pp. 131-135
Author(s):  
K. E Makhkamov ◽  
Miralib M. Azizov ◽  
T. A Vervekina ◽  
D. A Nishonov
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Pituitary Adenomas ◽  
Pituitary Apoplexy ◽  
Biological Marker ◽  
Vascular Endothelial ◽  
Hormonal Activity ◽  
Vegf Expression ◽  
Cystic Component ◽  
Endothelial Growth Factor ◽  
The Relationship

Aim. Despite the fact that the pituitary adenoma is a relatively benign tumor, sometimes the course of the disease is complicated by intramedullary hemorrhage. In the world literature there are single data on the molecular mechanism of hemorrhage in the adenomas of the pituitary gland. Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis and permeability of the endothelium in various brain tumors. There was made an analysis of the relationship between pituitary apoplexy and VEGF expression in pituitary adenomas. Material and methods. Immunohistochemical investigation of the level of expression of the molecular-biological marker - VEGF was performed with the use of monoclonal antibodies with the method of semiquantitative analysis in 30 pituitary adenoma patients. In the clinical study data about the age, gender, hormonal activity and X-ray study were studied. There was executed a statistical analysis of the relationship between clinical diagnostic data and VEGF expression. Results. Hormonal active tumors were detected in 12 (40%) cases, intratumoral hemorrhage - in 16 (53.3%), adenomas with cystic component - in 7 (23.3%) and invasion of cavernous sinus - in 22 (73.3%) of cases. Expression of VEGF was observed in 11 cases (36.6%). Based on the analysis the expression of VEGF was found to be closely related to pituitary apoplexy (PA) in pituitary adenomas (p < 0.001). However, there was no statistically significant relationship between VEGF and age, sex, tumor size, hormonal activity, cystic component presence, invasive tumor growth (p > 0.05). Conclusion. It was found that immunohistochemical examination of the level of expression of a molecular biological marker VEGF can be used in the evaluation of the prognosis of the disease or the identification of a risk group with a high probability of the development of pituitary apoplexy and recurrence of tumor growth.

scholarly journals Correlation of endothelial cell proliferation with vascular endothelial growth factor in endometrium of women with menorrhagia

2017 ◽  
Vol 5 (5) ◽  
pp. 2034
Author(s):  
Kiran B. Mehra ◽  
Nitin M. Gangane ◽  
Deepti R. Joshi
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Proliferation ◽  
Endothelial Cell Proliferation ◽  
P Value ◽  
Vascular Endothelial ◽  
Luminal Surface ◽  
Vegf Expression ◽  
Secretory Phase ◽  
Endothelial Proliferation ◽  
Endothelial Growth Factor

Background: Approximately 30% of women of reproductive age experience excessive blood loss during menstruation. In 50% of cases, menorrhagia has no underlying pathology. However, until recently, the only permanent cure for menorrhagia was hysterectomy. In this study we aim to determine the correlation of vascular endothelial growth factor (VEGF) expression with markers of endometrial endothelial cell proliferation like proliferating cell nuclear antigen (PCNA) and Cluster Determination (CD34).Methods: A total of 100 patients with history of menorrhagia were selected for study. Double Immunohistochemistry was performed on these endometrial biopsy sections. Proliferating endothelial cells were identified by an immunohistochemical double staining technique with PCNA and CD34. VEGF expression was also seen in endometrial biopsy.Results: In general, expression of both VEGF and PCNA was more in functional layer than basal layer in both menorrhagic patients as well as non menorrhagic patients.  When glandular cytoplasmic VEGF expression was compared with PCNA the association was statistically significant whereas completely opposite findings was seen with glandular luminal surface VEGF positivity but the association was statistically significant. In secretory phase (p-value<0.001) there was highly statistically significant association in PCNA grading with glandular luminal surface VEGF positivity whereas when we correlated PCNA with  cytoplasmic  glandular VEGF in secretory phase it was statistically significant (p-value<0.001).Conclusions: The endothelial proliferation was significantly higher in menorrhagia patients during late secretory phase of cycle than controls. We were able to demonstrate increased endothelial proliferation in patients in the premenstrual part of cycle.

scholarly journals Effects of high glucose on vascular endothelial growth factor expression in vascular smooth muscle cells

1997 ◽  
Vol 273 (5) ◽  
pp. H2224-H2231 ◽  
Author(s):  
Rama Natarajan ◽  
Wei Bai ◽  
Linda Lanting ◽  
Noe Gonzales ◽  
Jerry Nadler
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Endothelial ◽  
Ang Ii ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Mrna And Protein Expression ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF), in addition to its growth-promoting effects on endothelial cells, can also increase vascular permeability and monocyte migration. It has therefore been implicated in the pathogenic neovascularization associated with diabetic retinopathy and atherosclerosis. However, the factors regulating VEGF expression in the vascular wall are not fully understood. In this study, we examined the regulation of VEGF expression in vascular smooth muscle cells (VSMC) by hyperglycemia as well as by angiotensin II (ANG II). We also examined whether the 12-lipoxygenase (12-LO) product 12-hydroxyeicosatetraenoic acid (12-HETE) can alter VEGF expression, since 12-LO products of arachidonic acid have angiogenic properties, and ANG II as well as high glucose (HG, 25 mM) can increase 12-LO activity and expression in VSMC. Studies were carried out in human (HSMC) or porcine VSMC (PSMC), which were cultured for at least two passages under normal glucose (NG, 5.5 mM) or HG conditions. HG culture alone increased the expression of VEGF mRNA and protein in both HSMC and PSMC. Furthermore, ANG II treatment significantly induced VEGF mRNA and protein expression only in VSMC cultured in HG and not NG. In addition, 12-HETE significantly increased VEGF mRNA and protein expression in HSMC cultured in NG as well as in HG. Cells cultured in HG also secreted significantly greater amounts of VEGF into the culture medium. These results suggest that elevated VEGF production under HG conditions may play a role in the accelerated vascular disease observed in diabetes.

Expression of Vascular Endothelial Growth Factor in Human Monocyte/Macrophages Stimulated with Lipopolysaccharide

2001 ◽  
Vol 85 (01) ◽  
pp. 171-176 ◽  
Author(s):  
Hiroyuki Itaya ◽  
Hidemi Yoshida ◽  
Masayuki Koyama ◽  
Sohei Suzuki ◽  
Kei Satoh ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Map Kinase ◽  
Human Monocyte ◽  
P38 Map Kinase ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Endothelial Growth Factor

SummaryVascular endothelial growth factor (VEGF) is a mitogen for endothelial cells. We have studied the production of VEGF by human macrophages in response to lipopolysaccharide (LPS). Macrophages stimulated with LPS expressed VEGF mRNA and protein in concentration- and time-dependent manners. The LPS-induced expression of VEGF was inhibited by cycloheximide pretreatment, which suggested that synthesis of certain factor(s) is required for the LPS activity. The induction of VEGF was also suppressed by SB203580, an inhibitor of p38 mitogen-activated protein (MAP) kinase. These results suggest that the LPS-induced VEGF expression depends on the p38-mediated expression of c-Jun, which constitutes the AP-1 complex and binds to the AP-1 site in the VEGF promoter. Pretreatment of the cells with dexamethasone did not affect the LPS-induced upregulation of VEGF mRNA but strongly inhibited VEGF protein production, and the involvement of posttranscriptional regulation on VEGF expression by dexamethasone was suggested. The conditioned medium of LPS-stimulated macrophages enhanced the growth of cultured endothelial cells and it was inhibited by an antibody against VEGF. We conclude that macrophages produce VEGF in response to the stimulation with LPS, which may be partly mediated by the p38 MAP kinase pathway.

scholarly journals The Effect of HRE-Regulated VEGF Expression and Transfection on Neural Stem Cells in Rats

2020 ◽  
Vol 8 ◽  
Author(s):  
Bo Dou ◽  
Xiangrong Zheng ◽  
Danfeng Tan ◽  
Xixi Yin
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Target Cells ◽  
Vascular Endothelial ◽  
Rt Pcr ◽  
Vegf Gene ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Endothelial Growth Factor ◽  
Vegf Protein

In this study, we analyzed neural stem cells transfected with the HRE-VEGF gene in groups experiencing different periods of hypoxia. The results of RT-PCR showed that the expression of vascular endothelial growth factor (VEGF) mRNA gradually increased with the prolonged period of hypoxia (p &lt; 0.05). The results from the western-blot test showed that expression of the VEGF protein increased with as the period of hypoxia increased (p &lt; 0.05). The results of MTT combined with Elisa reagent showed that with the prolonged period of hypoxia, the secretion of VEGF protein increased, and that the proliferation of target cells and neural stem cells was better promoted (p &lt; 0.05). These results imply that HRE can safely and effectively regulate VEGF expression. By controlling the period of hypoxia, we can increase the expression level, and limit it in more safe values to avoid the possibility of cancer caused by the over-enhancement of proliferation of target cells due to the overexpression of the VEGF protein.

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