scholarly journals Oestrogen and progesterone receptors in the marmoset endometrium: changes during the ovulatory cycle, early pregnancy and after inhibition of vascular endothelial growth factor, GnRH or ovariectomy

Reproduction ◽  
2007 ◽  
Vol 134 (2) ◽  
pp. 341-353 ◽  
Author(s):  
Audrey Silvestri ◽  
Hamish M Fraser

Marmosets are widely used, but detailed studies on localisation of endometrial oestrogen receptors α and β (ERα and ERβ ), and the progesterone receptor (PR) are lacking. These receptors were localised and semi-quantitatively analysed throughout the ovulatory cycle, weeks 2, 3 and 4 of pregnancy and after treatment with GnRH antagonist, vascular endothelial growth factor (VEGF) Trap or ovariectomy. The PR in epithelial cells increased markedly between the mid- and late proliferative phases before declining in the mid-secretory phase and pregnancy. PR in stromal cells was present throughout the cycle and levels were maintained in pregnancy. ERα was present at the mid-proliferative phase and increased in glands at the late proliferative and early secretory phases, before declining at the late secretory phase and week 4 of pregnancy. Stromal ERα showed a similar trend, but decreased earlier, by the mid-secretory phase. ERβ was highly expressed in epithelial cells throughout the cycle and in pregnancy. In stroma, increases in ERβ expression were observed at the late proliferative phase with the staining index decreasing by half as the secretory phase progressed and in pregnancy. GnRH antagonist, VEGF Trap or ovariectomy caused significant reductions in PR and ERβ expression, but not in ERα when compared with the late proliferative phase of the normal cycle. Endothelial cells expressed ERβ , but not ERα or PR. It is concluded that the steroid receptor profile in the marmoset endometrium is generally similar to the human and should provide a useful model for studies on hormonal manipulation of the endometrium.

2002 ◽  
Vol 78 ◽  
pp. S283-S284
Author(s):  
Antonio Requena ◽  
Juan A Garcia-Velasco ◽  
Amparo Villasante ◽  
Marina Aragones ◽  
Rafaela Scheffer ◽  
...  

2000 ◽  
Vol 79 (1) ◽  
pp. 77-78 ◽  
Author(s):  
LUKAS HEFLER ◽  
ANDREAS OBERMAIR ◽  
PETER HUSSLEIN ◽  
CHRISTIAN KAINZ ◽  
CLEMENS TEMPFER

Endocrinology ◽  
2008 ◽  
Vol 149 (12) ◽  
pp. 6076-6083 ◽  
Author(s):  
Graham W. Aberdeen ◽  
Stanley J. Wiegand ◽  
Thomas W. Bonagura ◽  
Gerald J. Pepe ◽  
Eugene D. Albrecht

To assess whether there is a link between estrogen, vascular endothelial growth factor (VEGF), and early aspects of uterine angiogenesis, an acute temporal study was conducted in which ovariectomized baboons were pretreated with VEGF Trap, which sequesters endogenous VEGF, and administered estradiol at time 0 h. Serum estradiol levels approximated 500 pg/ml 4–6 h after estradiol administration. VEGF mRNA levels in endometrial glandular epithelial and stromal cells were increased to values 6 h after estradiol that were 3.74 ± 0.99-fold (mean ± se) and 5.70 ± 1.60-fold greater (P < 0.05), respectively, than at 0 h. Microvessel interendothelial cell tight junctions, which control paracellular permeability, were present in the endometrium at time 0 h, but not evident 6 h after estradiol administration. Thus, microvessel paracellular cleft width increased (P < 0.01, ANOVA) from 5.03 ± 0.22 nm at 0 h to 7.27 ± 0.48 nm 6 h after estrogen. In contrast, tight junctions remained intact, and paracellular cleft widths were unaltered in estradiol/VEGF Trap and vehicle-treated animals. Endometrial microvessel endothelial cell mitosis, i.e. percent Ki67+/Ki67− immunolabeled endothelial cells, increased (P < 0.05) from 2.9 ± 0.3% at 0 h to 21.4 ± 7.0% 6 h after estrogen treatment but was unchanged in estradiol/VEGF Trap and vehicle-treated animals. In summary, the estrogen-induced disruption of endometrial microvessel endothelial tight junctions and increase in endothelial cell proliferation were prevented by VEGF Trap. Therefore, we propose that VEGF mediates the estrogen-induced increase in microvessel permeability and endothelial cell proliferation as early steps in angiogenesis in the primate endometrium.


2021 ◽  
Author(s):  
Mi-Ra Kim ◽  
Bongkyu kim ◽  
Yunsu Na ◽  
Jingon Yoo ◽  
Se-Ho Kim ◽  
...  

AbstractAntiangiogenic therapies targeting vascular endothelial growth factor (VEGF)-A have been commonly used in clinics to treat cancers over the past decade. However, their clinical efficacy has been limited, with drawbacks including the acquisition of resistance and activation of compensatory pathways resulting from elevated circulating VEGF-B and placental growth factor (PlGF) levels. Thus, we developed a novel VEGF-Trap, KP-VR2, which can neutralize VEGF-A, VEGF-B, and PlGF to mediate these problems. KP-VR2 consists of two consecutive second Ig-like domains (D2s) of VEGF receptor 1 (VEGFR-1) fused to human IgG1 Fc. KP-VR2 showed more potent decoy activity than the current VEGF-Trap against VEGF and PlGF. Most importantly, two consecutive D2s of VEGFR-1 can generate two putative binding sites, resulting in a significant improvement in binding capacity. These advances resulted in stronger antitumor efficacy in implanted tumor models than aflibercept and bevacizumab. Overall, the results of this study highlight KP-VR2 as a promising therapeutic candidate for further clinical drug development.


2017 ◽  
Vol 60 (4) ◽  
pp. 515 ◽  
Author(s):  
GeokChin Tan ◽  
AbdFuaat Azliana ◽  
MohamadRazi Zainul-Rashid ◽  
SabrinaFlorence Chandramaya ◽  
WirdaIndah Farouk ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document