scholarly journals Effects of nicotine on Malassez' epithelial rest cells in early primary culture: cell proliferation and mRNA expression of heat shock protein 70 and vascular endothelial growth factor

2009 ◽  
Vol 13 (2) ◽  
pp. 41-45 ◽  
Author(s):  
Eri Nakagawa ◽  
Kenichi Matsuzaka ◽  
Shinichi Naruse ◽  
Kaoru Naito ◽  
Takashi Inoue
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Heat Shock ◽  
Heat Shock Protein 70 ◽  
Culture Cell ◽  
Vascular Endothelial ◽  
Primary Culture Cell ◽  
Early Primary ◽  
Endothelial Growth Factor

scholarly journals Rekombinan Vascular Endothelial Growth Factor-121 Menekan Ekspresi Heat Shock Protein-70 pada Plasenta Mencit Model Preeklampsia (VASCULAR ENDOTHELIAL GROWTH FACTOR-121 RECOMBINANT DEPRESSIS HEAT SHOCK PROTEIN-70 EXPRESSION IN PREECLAMPSIA MICE PLACENTA

2018 ◽  
Vol 18 (4) ◽  
pp. 589
Author(s):  
Sri Sulistyowati ◽  
Lungguk Helen Alfian Tanjung ◽  
Supriyadi Hari Respati ◽  
Soetrisno Soetrisno
Keyword(s):  
Oxidative Stress ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Heat Shock ◽  
Heat Shock Protein 70 ◽  
Vascular Endothelial ◽  
Model Group ◽  
Mice Model ◽  
Hsp 70 ◽  
Endothelial Growth Factor

Preeclampsia has remained a major cause of morbidity and maternal-perinatal mortality. Oxidative stress that occurs in preeclampsia increases HSP-70 expression. Therefore, VEGF therapy is expected to recover this oxidative stress. This research aimed to determine the role of VEGF-121 recombinant on HSP-70 expression in mice model of preeclampsia. This research was an explanatory study conducted at Animal Cage Experiment, Faculty of Veterinary Medicine, Airlangga University. The samples were 30 mice that were divided into 3 groups, namely a group of 10 normal pregnant mice, a group of 10 mice model of preeclampsia, and a group of 10 mice model of preeclampsia with VEGF-121 recombinant therapy. On the 16th day of gestation, HSP-70 expressions in the placenta of all mice were examined using immunohistochemical methods. The data were analyzed using Kruskall-Wallis test of SPSS program. The mean of HSP-70 expression in normal pregnancy group was 1.69 ± 0.68, in preeclampsia model group was 3.50 ± 0.95 with p = 0.00, and in preeclampsia model group with VEGF-121 recombinant therapy was 2.24 ± 0.84 with p = 0.00. In short, VEGF-121 recombinant has a role in lowering HSP-70 expression in mice placenta model of preeclampsia

scholarly journals The Involvement of Angiotensin Type 1 and Type 2 Receptors in Estrogen-Induced Cell Proliferation and Vascular Endothelial Growth Factor Expression in the Rat Anterior Pituitary

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Hanna Lawnicka ◽  
Dorota Ptasinska-Wnuk ◽  
Slawomir Mucha ◽  
Jolanta Kunert-Radek ◽  
Marek Pawlikowski ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Blood Vessels ◽  
Proliferation Index ◽  
Pituitary Cells ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Rat Pituitary ◽  
Endothelial Growth Factor

The aim of our study was to examine the involvement of renin-angiotensin system (RAS) in estrogen-induced lactotropes proliferation and vascular endothelial growth factor (VEGF) expression in rat pituitary. The study was performed on Fisher 344 rats underwent 8-day treatment with diethylstilboestrol (DES). The proliferation index (PCNA) and VEGF expression in pituitary sections were estimated using immunohistochemical methods. Treatment with DES increased the number of PCNA-positive cells, VEGF-positive cells, and VEGF-positive blood vessels in pituitary. Stimulatory effect of estrogen on cell proliferation and VEGF expression in blood vessels was attenuated by losartan, PD123319, and captopril. VEGF immunoreactivity in pituitary cells of DES-treated rats was decreased by AT1 antagonist and not changed by AT2 blocker and ACE inhibitor. Our findings suggest the involvement of RAS in DES-induced cell proliferation and VEGF expression in pituitary. Both the AT1 and AT2 receptors appear to mediate the estrogen-dependent mitogenic and proangiogenic effects in rat pituitary.

scholarly journals Successful inhibition of intracranial human glioblastoma multiforme xenograft growth via systemic adenoviral delivery of soluble endostatin and soluble vascular endothelial growth factor receptor-2

2008 ◽  
Vol 108 (5) ◽  
pp. 979-988 ◽  
Author(s):  
Oszkar Szentirmai ◽  
Cheryl H. Baker ◽  
Szofia S. Bullain ◽  
Ning Lin ◽  
Masaya Takahashi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Glioblastoma Multiforme ◽  
Tumor Growth ◽  
Growth Inhibition ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Treatment Groups ◽  
Endothelial Growth Factor

Object Glioblastoma multiforme (GBM) is characterized by neovascularization, raising the question of whether angiogenic blockade may be a useful therapeutic strategy for this disease. It has been suggested, however, that, to be useful, angiogenic blockade must be persistent and at levels sufficient to overcome proangiogenic signals from tumor cells. In this report, the authors tested the hypothesis that sustained high concentrations of 2 different antiangiogenic proteins, delivered using a systemic gene therapy strategy, could inhibit the growth of established intracranial U87 human GBM xenografts in nude mice. Methods Mice harboring established U87 intracranial tumors received intravenous injections of adenoviral vectors encoding either the extracellular domain of vascular endothelial growth factor receptor-2-Fc fusion protein (Ad-VEGFR2-Fc) alone, soluble endostatin (Ad-ES) alone, a combination of Ad-VEGFR2-Fc and Ad-ES, or immunoglobulin 1-Fc (Ad-Fc) as a control. Results Three weeks after treatment, magnetic resonance imaging-based determination of tumor volume showed that treatment with Ad-VEGFR2-Fc, Ad-ES, or Ad-VEGFR2-Fc in combination with Ad-ES, produced 69, 59, and 74% growth inhibition, respectively. Bioluminescent monitoring of tumor growth revealed growth inhibition in the same treatment groups to be 62, 74, and 72%, respectively. Staining with proliferating cell nuclear antigen and with terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling showed reduced tumor cell proliferation and increased apoptosis in all antiangiogenic treatment groups. Conclusions These results suggest that systemic delivery and sustained production of endostatin and soluble VEGFR2 can slow intracranial glial tumor growth by both reducing cell proliferation and increasing tumor apoptosis. This work adds further support to the concept of using antiangiogenesis therapy for intracranial GBM.

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