scholarly journals Relaxin (RLX) and estrogen affect estrogen receptor α, vascular endothelial growth factor, and RLX receptor expression in the neonatal porcine uterus and cervix

Reproduction ◽  
2008 ◽  
Vol 135 (5) ◽  
pp. 705-712 ◽  
Author(s):  
Wenbo Yan ◽  
Joseph Chen ◽  
Anne A Wiley ◽  
Bethany D Crean-Harris ◽  
Frank F Bartol ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Estrogen Receptor ◽  
Growth Factor ◽  
Protein Content ◽  
Reproductive Tract ◽  
Female Reproductive Tract ◽  
Receptor Expression ◽  
Vascular Endothelial ◽  
Wet Weight ◽  
Endothelial Growth Factor

The porcine female reproductive tract undergoes estrogen receptor (ER) α-dependent development after birth (postnatal day=PND 0), the course of which can determine adult uterine function. Uterotrophic effects of relaxin (RLX) in the porcine neonate are age specific and may involve ER activation. Here, objectives were to determine effects of RLX and estrogen administered from birth on uterine and cervical growth and expression of ERα, vascular endothelial growth factor (VEGF), and the RLX receptor (RXFP1). On PND 0, gilts were treated with the antiestrogen ICI 182 780 (ICI) or vehicle alone and, 2 h later, were given estradiol-17β (E) or porcine RLX for 2 days. Neither RLX nor E affected uterine wet weight or protein content on PND 2. However, RLX, but not E, increased cervical wet weight and protein content when compared with controls. Pretreatment with ICI did not inhibit RLX-stimulated cervical growth. Uterine and cervical ERα increased in response to RLX, but not E. Both RLX and E increased VEGF in the uterus and cervix on PND 2. Pretreatment with ICI increased VEGF in both tissues and increased RLX-induced cervical VEGF. In the uterus E, but not RLX, increased RXFP1 mRNA. In the cervix, E increased RXFP1 gene expression whereas RLX decreased it. Results indicate that the neonatal uterus and cervix are sensitive to E and RLX and that growth responses to RLX in these tissues differ by PND 2. Effects of RLX on uterine and cervical ERα and VEGF expression may be important for neonatal reproductive tract development.

Vascular Endothelial Growth Factor Isoform and Receptor Expression During Compensatory Lung Growth

2010 ◽  
Vol 160 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Tim Jancelewicz ◽  
Erich J. Grethel ◽  
Cheryl J. Chapin ◽  
Matthew S. Clifton ◽  
Kerilyn K. Nobuhara
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Receptor Expression ◽  
Vascular Endothelial ◽  
Lung Growth ◽  
Compensatory Lung Growth ◽  
Endothelial Growth Factor

Differences in vascular endothelial growth factor receptor expression and correlation with the degree of enhancement in medulloblastoma

2014 ◽  
Vol 14 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Shawn L. Hervey-Jumper ◽  
Hugh J. L. Garton ◽  
Darryl Lau ◽  
David Altshuler ◽  
Douglas J. Quint ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Perioperative Complications ◽  
Prognostic Significance ◽  
Growth Factor Receptor ◽  
Extent Of Resection ◽  
Receptor Expression ◽  
Vascular Endothelial ◽  
Significant Difference ◽  
Endothelial Growth Factor

Object Vascular endothelial growth factor (VEGF) is the major proangiogenic factor in many solid tumors. Vascular endothelial growth factor receptor (VEGFR) is expressed in abundance in pediatric patients with medulloblastoma and is associated with tumor metastasis, poor prognosis, and proliferation. Gadolinium enhancement on MRI has been suggested to have prognostic significance for some tumors. The association of VEGF/VEGFR and Gd enhancement in medulloblastoma has never been closely examined. The authors therefore sought to evaluate whether Gd-enhancing medulloblastomas have higher levels of VEGFR and CD31. Outcomes and survival in patients with enhancing and nonenhancing tumors were also compared. Methods A retrospective analysis of patients with enhancing, nonenhancing, and partially enhancing medulloblastomas was performed. Primary end points included risk stratification, extent of resection, and perioperative complications. A cohort of 3 enhancing and 3 nonenhancing tumors was selected for VEGFR and CD31 analysis as well as microvessel density measurements. Results Fifty-eight patients were analyzed, and 20.7% of the medulloblastomas in these patients were nonenhancing. Enhancing medulloblastomas exhibited strong VEGFR1/2 and CD31 expression relative to nonenhancing tumors. There was no significant difference in perioperative complications or patient survival between the 2 groups. Conclusions These results suggest that in patients with medulloblastoma the presence of enhancement on MRI may correlate with increased vascularity and angiogenesis, but does not correlate with worse patient prognosis in the short or long term.

Vascular Endothelial Growth Factor Family and Receptor Expression in Human Choroidal Neovascular Membranes

2002 ◽  
Vol 64 (1) ◽  
pp. 162-169 ◽  
Author(s):  
Atsushi Otani ◽  
Hitoshi Takagi ◽  
Hideyasu Oh ◽  
Shinji Koyama ◽  
Yuichiro Ogura ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Receptor Expression ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Estrogen Receptor-α Overexpression Suppresses 17β-Estradiol-Mediated Vascular Endothelial Growth Factor Expression and Activation of Survival Kinases

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 3881-3889 ◽  
Author(s):  
Shameena Bake ◽  
Lijiang Ma ◽  
Farida Sohrabji
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Estrogen Receptor ◽  
Growth Factors ◽  
Growth Factor ◽  
Cell Line ◽  
Female Rats ◽  
High Dose ◽  
Vascular Endothelial ◽  
17Β Estradiol ◽  
Endothelial Growth Factor

Estrogen and its receptors influence growth and differentiation by stimulating the production and secretion of growth factors. Our previous studies indicate an increased expression of estrogen receptor (ER)-α and decreased growth factor synthesis in the olfactory bulb of reproductive senescent female rats as compared with young animals. The present study tests the hypothesis that abnormal overexpression of ERα contributes to decreased growth factor synthesis. We developed the HeLa-Tet-On cell line stably transfected with ERα (HTERα) that expresses increasing amounts of ERα with increasing doses of doxycycline (Dox). Increasing doses of Dox had no effect on vascular endothelial growth factor (VEGF) secretion in HTERα cells. However, in the presence of 40 nm 17β-estradiol, VEGF secretion increased in low-dose Dox-exposed HTERα cultures, which was attenuated by the ERα antagonist, 1,3-Bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]1H-pyrazole dihydrochloride. However, at high-dose Dox and, consequently, high ERα levels, estradiol failed to increase VEGF. In the HeLa X6 cell line in which the Tet-On construct is upstream of an unrelated gene (Pitx2A), estradiol failed to induce VEGF at any Dox dose. Furthermore, in the HTERα cell line, estradiol selectively down-regulates phospho-ERK2 and phospho-Akt at high ERα expression. This study clearly demonstrates that the dose of receptor critically mediates estradiol’s ability to regulate growth factors and survival kinases. The present data also support the hypothesis that 17β-estradiol treatment to an ERα overexpressing system, such as the senescent brain, could reverse the normally observed beneficial effect of estrogen.

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