scholarly journals Effects of GnRH antagonist treatment on follicular development and angiogenesis in the primate ovary

2004 ◽  
Vol 183 (1) ◽  
pp. 1-17 ◽  
Author(s):  
P D Taylor ◽  
S G Hillier ◽  
H M Fraser
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Gnrh Antagonist ◽  
Follicular Development ◽  
Follicular Phase ◽  
Endothelial Cell Proliferation ◽  
Vascular Density ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Paracrine Factors

Angiogenesis is required for normal follicular development but the role of gonadotrophins in the control of follicular angiogenesis remains to be elucidated. This study investigated the effects of treatment with GnRH antagonist in vivo on follicular development and angiogenesis in the marmoset. GnRH antagonist was administered on either follicular day 0 or day 5 of the 10-day follicular phase with ovaries collected on day 10. Ovaries from control marmosets were studied at day 5 (mid follicular phase) and day 10 (periovulatory period). Ovaries were fixed, serial sectioned and subjected to morphological analysis and immunocytochemistry to determine cell proliferation and follicular endothelial cell area and in situ hybridization to assess changes in expression of vascular endothelial growth factor (VEGF). Treatment with GnRH antagonist from day 0–10 resulted in an absence of dominant preovulatory follicles seen in controls. In the remaining tertiary follicles granulosa, theca and endothelial cell proliferation was reduced, resulting in a minor reduction in vascular density. However, VEGF mRNA expression was unaffected by treatment. Treatment from day 5–10 did not prevent development of ovulatory size follicles, but they were atretic and lacked VEGF mRNA. These results suggest that while VEGF expression in the preovulatory follicle is under gonadotrophic control it is not dependent on normal gonadotrophin secretion in tertiary follicles, indicating that there are other paracrine factors regulating VEGF expression in the developing ovarian follicle.

Low-dose photodynamic therapy increases endothelial cell proliferation and VEGF expression in nude mice brain

2005 ◽  
Vol 20 (2) ◽  
pp. 74-79 ◽  
Author(s):  
Xuepeng Zhang ◽  
Feng Jiang ◽  
Zheng Gang Zhang ◽  
Steven N Kalkanis ◽  
Xin Hong ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Photodynamic Therapy ◽  
Endothelial Cell ◽  
Nude Mice ◽  
Low Dose ◽  
Endothelial Cell Proliferation ◽  
Vegf Expression ◽  
Mice Brain

scholarly journals KCa3.1 channel blockade attenuates microvascular remodelling in a large animal model of bleomycin-induced pulmonary fibrosis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Habtamu B. Derseh ◽  
Sasika N. Vithana Dewage ◽  
Kopiyawaththage U. E. Perera ◽  
Charles N. Pagel ◽  
Emmanuel Koumoundouros ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Pulmonary Fibrosis ◽  
Large Animal Model ◽  
Endothelial Cell Proliferation ◽  
Pulmonary Vasculature ◽  
Large Animal ◽  
Vascular Remodelling ◽  
Vegf Expression ◽  
Endothelial Growth Factor

AbstractIdiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with limited therapeutic options and poor prognosis. IPF has been associated with aberrant vascular remodelling, however the role of vascular remodelling in pulmonary fibrosis is poorly understood. Here, we used a novel segmental challenge model of bleomycin-induced pulmonary fibrosis in sheep to evaluate the remodelling of the pulmonary vasculature, and to investigate the changes to this remodelling after the administration of the KCa3.1 channel inhibitor, senicapoc, compared to the FDA-approved drug pirfenidone. We demonstrate that in vehicle-treated sheep, bleomycin-infused lung segments had significantly higher blood vessel density when compared to saline-infused control segments in the same sheep. These microvascular density changes were significantly attenuated by senicapoc treatment. The increases in vascular endothelial growth factor (VEGF) expression and endothelial cell proliferation in bleomycin-infused lung segments were significantly reduced in sheep treated with the senicapoc, when compared to vehicle-treated controls. These parameters were not significantly suppressed with pirfenidone treatment. Senicapoc treatment attenuated vascular remodelling through inhibition of capillary endothelial cell proliferation and VEGF expression. These findings suggest a potential new mode of action for the novel drug senicapoc which may contribute to its efficacy in combatting pulmonary fibrosis.

scholarly journals Mast cell degranulation in rat uterine cervix during pregnancy correlates with expression of vascular endothelial growth factor mRNA and angiogenesis

Reproduction ◽  
2007 ◽  
Vol 133 (5) ◽  
pp. 1045-1055 ◽  
Author(s):  
V L Bosquiazzo ◽  
J G Ramos ◽  
J Varayoud ◽  
M Muñoz-de-Toro ◽  
E H Luque
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Mrna Expression ◽  
Relative Abundance ◽  
Splice Variants ◽  
Serum Levels ◽  
Endothelial Cell Proliferation ◽  
Vegf Mrna ◽  
Pregnant Rats ◽  
Vegf Mrna Expression

Vascular growth of the uterine cervix during pregnancy is associated with mast cell (MC) degranulation. To better understand the mechanism underlying this process, uterine cervices of intact pregnant rats were dissected and endothelial cell proliferation was measured by a bromodeoxyuridine incorporation technique. Total vascular endothelial growth factor (VEGF) mRNA expression and the relative abundance of VEGF splice variants (120, 164, and 188) were determined by RT-PCR. VEGF protein expression was evaluated by immunohistochemistry. To investigate the role of MCs on cervical angiogenesis, a second set of pregnant animals were treated with an MC stabilizer (disodium cromoglycate) to inhibit MC degranulation. Furthermore, 17β-estradiol (E2) serum levels were established by RIA. In intact pregnant rats, VEGF mRNA expression was positively correlated with endothelial cell proliferation and circulating E2levels. All selected splice variants ofVEGFgene were detected and their relative abundance did not show any change throughout pregnancy. Animals treated with disodium cromoglycate showed a decrease in endothelial cell proliferation and in VEGF mRNA expression compared with controls. Relative abundance of VEGF mRNA splice variants and E2serum levels showed no differences between these experimental groups. These results show a time-dependent correlation between VEGF mRNA expression and E2serum levels in the uterine cervix of intact pregnant rats, while MC stabilizer-treated animals reduced the VEGF expression without modifying E2serum levels. We suggest that cervical angiogenesis during pregnancy could be regulated by a mechanism which involves endogenous E2and chemical mediators stored in MC granules via a VEGF-dependent pathway.

Angiogenic Effects of the Extracts from Chinese Herbs: Angelica and ChuanXiong

2008 ◽  
Vol 36 (03) ◽  
pp. 541-554 ◽  
Author(s):  
Hua Meng ◽  
Jun Guo ◽  
Ji-Yuan Sun ◽  
Jian-Ming Pei ◽  
Yue-Min Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Acute Treatment ◽  
Chinese Herbs ◽  
Endothelial Cell Proliferation ◽  
Control Group ◽  
Oxygen Balance ◽  
Vegf Expression ◽  
Peripheral Ischemia

Angelica and ChuanXiong are used to cure ischemic heart disease in China. Previous studies found that these two herbs could increase myocardial blood flow, oxygen-supply and keep myocardial oxygen balance, etc. However, the mechanisms of angiogenic effects of these two herbs are not well-known. The purpose of this study was to assess the effects of Angelica and ChuanXiong on vascular endothelial growth factor (VEGF) expression in rat myocardial infarction, on endothelial cell proliferation and quantity of vessels on chick embryo chorioallantoic membrane (CAM). In this study, rats were divided randomly into either pre-treatment or acute-treatment group and sacrificed at the end of the treatments. VEGF expression using Western blot analysis was significantly increased in the groups pre-treated with ChuanXiong and Angelica when compared to the control group ( p < 0.05). There was significant increase in VEGF expression in the rats treated acutely with Angelica ( p < 0.05). In the contrary, the rats treated with ChuanXiong showed a decrease in VEGF expression when compared to the acute-treatment control group ( p < 0.05). Similar results were observed in immunohistochemistry of VEGF expression in the myocardia. Our study also demonstrated that these two herbs significantly enhanced endothelial cell proliferation ( p < 0.05) and revascularity in CAM ( p < 0.05). The data showed that Angelica and ChuanXiong could affect VEGF expression in rat myocardial infarction, promote endothelial cell proliferation and stimulate quantity of vessels on CAM model. The results suggest that Angelica and ChuanXiong have angiogenic effects, and may provide some mechanisms for the treatment of myocardial infarction and peripheral ischemia.

scholarly journals Fibroblast Growth Factor-2 (FGF-2) Induces Vascular Endothelial Growth Factor (VEGF) Expression in the Endothelial Cells of Forming Capillaries: An Autocrine Mechanism Contributing to Angiogenesis

1998 ◽  
Vol 141 (7) ◽  
pp. 1659-1673 ◽  
Author(s):  
Graziano Seghezzi ◽  
Sundeep Patel ◽  
Christine J. Ren ◽  
Anna Gualandris ◽  
Giuseppe Pintucci ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Vascular Endothelial Cell ◽  
Membrane Receptors ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Vegf Mrna

FGF-2 and VEGF are potent angiogenesis inducers in vivo and in vitro. Here we show that FGF-2 induces VEGF expression in vascular endothelial cells through autocrine and paracrine mechanisms. Addition of recombinant FGF-2 to cultured endothelial cells or upregulation of endogenous FGF-2 results in increased VEGF expression. Neutralizing monoclonal antibody to VEGF inhibits FGF-2–induced endothelial cell proliferation. Endogenous 18-kD FGF-2 production upregulates VEGF expression through extracellular interaction with cell membrane receptors; high-Mr FGF-2 (22–24-kD) acts via intracellular mechanism(s). During angiogenesis induced by FGF-2 in the mouse cornea, the endothelial cells of forming capillaries express VEGF mRNA and protein. Systemic administration of neutralizing VEGF antibody dramatically reduces FGF-2-induced angiogenesis. Because occasional fibroblasts or other cell types present in the corneal stroma show no significant expression of VEGF mRNA, these findings demonstrate that endothelial cell-derived VEGF is an important autocrine mediator of FGF-2-induced angiogenesis. Thus, angiogenesis in vivo can be modulated by a novel mechanism that involves the autocrine action of vascular endothelial cell-derived FGF-2 and VEGF.

Inhibition of adenosine kinase induces expression of VEGF mRNA and protein in myocardial myoblasts

2000 ◽  
Vol 279 (5) ◽  
pp. H2116-H2123 ◽  
Author(s):  
Jian-Wei Gu ◽  
Bruce R. Ito ◽  
Amanda Sartin ◽  
Nan Frascogna ◽  
Michael Moore ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Protein Expression ◽  
Kinase Inhibitor ◽  
Umbilical Vein ◽  
Adenosine Kinase ◽  
Endothelial Cell Proliferation ◽  
Cell Protein ◽  
Vegf Mrna ◽  
Vegf Protein

We tested whether increased endogenous adenosine produced by the adenosine kinase inhibitor GP-515 (Metabasis Therapeutics) can induce vascular endothelial growth factor (VEGF) expression in cultured rat myocardial myoblasts (RMMs). RMMs were cultured for 18 h in the absence (control) and presence of GP-515, adenosine (Ado), adenosine deaminase (ADA), or GP-515 + ADA. GP-515 (0.2–200 μM) caused a dose-related increase in VEGF protein expression (1.99–2.84 ng/mg total cell protein); control VEGF was 1.84 ± 0.05 ng/mg. GP-515 at 2 and 20 μM also increased VEGF mRNA by 1.67- and 1.82-fold, respectively. ADA (10 U/ml) decreased baseline VEGF protein levels by 60% and completely blocked GP-515 induction of VEGF. Ado (20 μM) and GP-515 (20 μM) caused a 59 and 39% increase in VEGF protein expression and a 98 and 33% increase in human umbilical vein endothelial cell proliferation, respectively, after 24 h of exposure. GP-515 (20 μM) had no effect on VEGF protein expression during severe hypoxia (1% O2) but increased VEGF by an additional 27% during mild hypoxia (10% O2). These results indicate that raising endogenous levels of Ado through inhibition of adenosine kinase can increase the expression of VEGF and stimulate endothelial cell proliferation during normoxic and hypoxic conditions.

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