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 < 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 < 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 < 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.

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.

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.

scholarly journals Direct Stimulation of Adult Neural Stem Cells In Vitro and Neurogenesis In Vivo by Vascular Endothelial Growth Factor

2006 ◽  
Vol 14 (3) ◽  
pp. 237-248 ◽  
Author(s):  
Anne Schänzer ◽  
Frank-Peter Wachs ◽  
Daniel Wilhelm ◽  
Till Acker ◽  
Christiana Cooper-Kuhn ◽  
...  
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Neural Stem Cells ◽  
Vascular Endothelial ◽  
Direct Stimulation ◽  
Endothelial Growth Factor ◽  
Stimulation Of

scholarly journals All-Trans Retinoic Acid Inhibits Vascular Endothelial Growth Factor Expression in a Cell Model of Neutrophil Activation

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1264-1270 ◽  
Author(s):  
Meng Kian Tee ◽  
Jean-Louis Vigne ◽  
Robert N. Taylor
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Retinoic Acid ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Vegf Gene ◽  
Vegf Mrna ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Neutrophil Differentiation ◽  
Endothelial Growth Factor

Infiltrating neutrophil granulocytes are a particularly rich source of vascular endothelial growth factor (VEGF) in the endometrium and may contribute to the angiogenesis of endometriosis lesions. The objective of this study is to evaluate the expression and regulation of VEGF in endometrial neutrophils and in a model of neutrophil differentiation relevant to endometriosis. Immunohistochemistry was performed on endometriosis patient biopsies and cultured neutrophil-like HL-60 cells were assessed. The study was set in a reproductive biology division within an academic medical center. Endometrial biopsies were performed on women with endometriosis and HL-60 cells were treated with all-trans retinoic acid (atRA) and dimethyl sulfoxide in vitro. Immunofluorescence histochemistry, VEGF mRNA and protein quantification, and transfection studies of VEGF gene promoter-luciferase constructs were all main outcome measures. Immunofluorescence studies verified the presence of neutrophils in eutopic endometrium from women with endometriosis. Examination of the regulation of VEGF using differentiated HL-60 cells as a model, revealed that atRA induced a dose- and time-dependent suppression of VEGF mRNA and protein. Transient transfection, truncation, EMSA, and site-directed mutagenesis of human VEGF promoter-luciferase constructs in HL-60 cells indicated that atRA repressed VEGF gene transcription via a direct repeat 1 element located between −443 and −431 bp relative to the transcription initiation site. Because retinoic acid is synthesized de novo in endometrial cells under the influence of progesterone, our findings suggest that the up-regulated VEGF and angiogenesis in tissue from women with endometriosis may reflect failure of neutrophil differentiation in these cases, and provide a rationale for retinoid therapy in this condition.

MicroRNA-199a Protects Diabetic Retinopathy Under Streptozotocin Conditions by Vascular Endothelial Growth Factor (VEGF)

2020 ◽  
Vol 10 (3) ◽  
pp. 408-412
Author(s):  
Xuemei Wu ◽  
Liang Hui
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Cell Damage ◽  
Vascular Endothelial ◽  
Rt Pcr ◽  
Vegf Expression ◽  
Inflammatory Stress ◽  
Over Expression ◽  
Vegf Signaling ◽  
Endothelial Growth Factor

Inflammatory stress and angiogenesis participate in diabetic retinopathy. miR-199α could inhibit the elevation of wound angiogenesis by suppressing TNF-α and NF-κB pathway. The mechanism of miR-199a in streptozotocin (STZ)-induced cell damage was assessed by ELLISA kit, western blotting, real-time RT-PCR. Reactive oxygen Species (ROS) was measured by flow cytometry. The over expression of miR-199a decreased the STZ-stimulated oxidative stress, inflammatory response, as well as VEGF expression. In conclusion, our results validated that overexpression of miR-199a protects RMECs from STZ-induced inflammation, oxidative stress and angiogenesis by targeting, at least partly, the VEGF signaling.

Expression of vascular endothelial growth factor and its receptors in rat neural stem cells

2003 ◽  
Vol 344 (3) ◽  
pp. 165-168 ◽  
Author(s):  
Martin H. Maurer ◽  
Wolf K.C. Tripps ◽  
Robert E. Feldmann ◽  
Wolfgang Kuschinsky
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Neural Stem Cells ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Basic Fibroblast Growth Factor-Mediated Overexpression of Vascular Endothelial Growth Factor in 1F6 Human Melanoma Cells is Regulated by Activation of PI-3K and p38 MAPK

2009 ◽  
Vol 31 (3) ◽  
pp. 179-190
Author(s):  
Dennis Fontijn ◽  
Linda J. W. Bosch ◽  
Monique C. A. Duyndam ◽  
Maria P. A. van Berkel ◽  
Maarten L. Janmaat ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Protein Secretion ◽  
Human Melanoma ◽  
Vascular Endothelial ◽  
Fibroblast Growth ◽  
Vegf Mrna ◽  
Endothelial Growth Factor ◽  
Vegf Protein

Background: 1F6 human melanoma xenografts overexpressing either the 18 kD (18kD) form or all (ALL) forms of human basic fibroblast growth factor (bFGF) demonstrate an abundant number of microvessels and accelerated growth. We now examined whether bFGF mediates vascular endothelial growth factor (VEGF) expression.Methods: Quantitative RT-PCR was used to determine bFGF and VEGF mRNA, VEGF protein secretion was measured by ELISA and VEGF promoter activation was assessed by a dual luciferase activity assay. Western blot was carried out to detect phosphorylation of bFGF-regulated target proteins.Results: In 1F6-18kD and 1F6-ALL clones VEGF mRNA was increased 4- to 5-fold and VEGF protein secretion was highly stimulated due to activation of the VEGF promotor. PI-3K, p38 MAPK and ERK1/2 MAPK pathways were activated, while inhibition of PI-3K or p38 resulted in, respectively, 55% and up to 70% reduction of VEGF mRNA overexpression. A concurrent 60% decrease in VEGF protein secretion was mostly apparent upon inhibition of PI-3K. Inhibition of ERK1/2 hardly affected VEGF mRNA or protein secretion. Two unselected human melanoma cell lines with high metastatic potential contained high bFGF and VEGF, while three non- or sporadically metastatic cell lines displayed low bFGF and VEGF.Conclusion: These data indicate that stimulation of VEGF protein secretion in response to bFGF overexpression may contribute to increased vascularization and enhanced aggressiveness in melanoma.

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.

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