scholarly journals The carriers of the A/G-G/G allelic combination of the c.2039 A>G and c.-29 G>A FSH receptor polymorphisms retrieve the highest number of oocytes in IVF/ICSI cycles

2016 ◽  
Vol 34 (2) ◽  
pp. 263-273 ◽  
Author(s):  
Adolfo Allegra ◽  
Angelo Marino ◽  
Stefania Raimondo ◽  
Antonio Maiorana ◽  
Salvatore Gullo ◽  
...  
2006 ◽  
Vol 52 (1) ◽  
pp. 15-19 ◽  
Author(s):  
T. Ishikawa ◽  
M. Fujisawa ◽  
J. Tapanainen

2020 ◽  
Vol 71 (10) ◽  
pp. 212-217
Author(s):  
Adina-Elena Tanase ◽  
Roxana Popescu ◽  
Mircea Onofriescu ◽  
Roxana Daniela Matasariu

Endometriosis is a disease very common nowadays affecting 1-2% of the female population, by estrogen-dependent mechanism. The identification of mutations in the gene encoding for the FSH receptor (FSHR) has been reported since 1995. Physiology teaches us that follicle-stimulating hormone (FSH) is a hormone that is vital in the steroidogenesis regulation mechanisms, while FSH receptor (FSHR) activation helps to promote folliculogenesis and estrogensynthesis. Therefore, studies to show if there are any correlations between endometriosis and FSHR are acquired. Genotyping of FSHR gene polymorphisms were performed using PCR - Restriction Fragment Length Polymorphism (PCR-RFLP) analysis. We analysed a total of 78 patients, 44 infertile patients with endometriosis and 34 controls (non-infertile, pregnant patients). The endometriosis group included women with diagnosis of endo-metriosis confirmed by laparoscopy and /or laparotomy and histological evidence of disease with the endometriosis staging according to American Society for Reproductive Medicine (ASRM). Corroborated with the severity of endometriosis, A919G and A2039G tests found that 71.4% of the M (GG) results were associated with primary infertility, not statistically significant (p=0.994) and 42.9% of the total M results had moderate or severe forms of endometriosis (p = 0.185). The genetic involvement in different pathologies such as endometriosis, has yet to be understood, but knowing more about its mechanism, will help physician target the disease at a more profound level.


2019 ◽  
Vol 19 (14) ◽  
pp. 1719-1727
Author(s):  
Zhuandi Gong ◽  
Xiaoyun Shen ◽  
Juan Yang ◽  
Luju Lai ◽  
Suocheng Wei

Background: FSH Receptor Binding Inhibitor (FRBI) blocked the binding of FSH to FSHR. Our initial study revealed FRBI reduced the maturation rate, enhanced the apoptosis of sheep Cumulus-Oocyte Complex (COCs). Little is known about whether FRBI modulates ERβ and FSHR levels in the normal uterine and cancerous tissues. The present study aimed to evaluate the FRBI effects on the expressions of Estrogen Receptor-beta (ERβ) and FSH receptor (FSHR) in the uteri. Methods: Methods: 150 mice were assigned to FRBI+FSH (COM), FSH and control groups (CG). Mice of COM-1, COM-2 and COM-3 groups were simultaneously intramuscularly injected with 500, 750 and 1000 µg FRBI with 10 IU FSH, respectively for five days. Western blotting and qPCR were utilized to determine the expression of ERβ and FSHR. Results: In comparison with FSH group, uterine lumen and glands of COM groups became narrow. The uterine wall and endometrial epithelium were thinned, and uterine lumen became narrow. Epithelial cells were decreased. Uterine wall thicknesses of COM-1, COM-2 and COM-3 groups were reduced by 6.49%, 14.89% and 15.69% on day 30 as compared with FSH group. Uterine perimetrium thicknesses of COM-1, COM-2 and COM-3 groups were reduced by 16.17%, 17.93% and 19.92% on day 20 in comparison with FSH group. Levels of FSHR mRNAs and proteins of COM-1, COM-2 and COM-3 groups were less than FSH group on days 20 and 30 (P<0.05). ERβ protein of COM-3 group was less than FSH group. Serum estradiol (E2) and FSH concentrations of COM-2 and COM-3 were lower than that of FSH group on day 30. Conclusion: FRBI could decrease UWT and UPT, also block the uterine development, decline expression levels of ERβ and FSHR protein. Additionally, FRBI reduced the secretion of secretion of FSH and E2. Downregulating expression of FSHR and ERβ may be a potential treatment regimen for cervical cancer patients.


2001 ◽  
Vol 17 (2) ◽  
pp. 120-121
Author(s):  
B Klauß-Perschke ◽  
H O Hoppen ◽  
S Schlote

FEBS Journal ◽  
2020 ◽  
Author(s):  
Antara A. Banerjee ◽  
Shaini Joseph ◽  
Smita D. Mahale
Keyword(s):  

2005 ◽  
Vol 142 (1-2) ◽  
pp. 34-43 ◽  
Author(s):  
Jan Bogerd ◽  
Joke C.M. Granneman ◽  
Rüdiger W. Schulz ◽  
Henry F. Vischer
Keyword(s):  

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3925-3930 ◽  
Author(s):  
Xiuyan Feng ◽  
Meilin Zhang ◽  
Rongbin Guan ◽  
Deborah L. Segaloff

The LH receptor (LHR) and FSH receptor (FSHR) are each G protein-coupled receptors that play critical roles in reproductive endocrinology. Each of these receptors has previously been shown to self-associate into homodimers and oligomers shortly after their biosynthesis. As shown herein using bioluminescence resonance energy transfer to detect protein-protein interactions, our data show that the LHR and FSHR, when coexpressed in the same cells, specifically heterodimerize with each other. Further experiments confirm that at least a portion of the cellular LHR/FSHR heterodimers are present on the cell surface and are functional. We then sought to ascertain what effects, if any, heterodimerization between the LHR and FSHR might have on signaling. It was observed that when the LHR was expressed under conditions promoting the heterodimerization with FSHR, LH or human chorionic gonadotropin (hCG) stimulation of Gs was attenuated. Conversely, when the FSHR was expressed under conditions promoting heterodimerization with the LHR, FSH-stimulated Gs activation was attenuated. These results demonstrate that the coexpression of the LHR and FSHR enables heterodimerizaton between the 2 gonadotropin receptors and results in an attenuation of signaling through each receptor.


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