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1.
Egyptian Journal of Hospital Medicine [The]. 2017; 67 (1): 352-358
in English | IMEMR | ID: emr-189187

ABSTRACT

Background: Recent studies have implicated a role for inhibin alpha [INH alpha] gene abnormalities in the etiology of premature ovarian failure [POF].The present study aimed at demonstrating the possibility that -16C>T polymorphism of INH alpha gene may enhance susceptibility to this disease among Egyptian women undergoingt in-vitro fertilization[IVF] technique


Methods: A total of 50 POF Egyptian women at age [31.5 +/- 7.3] and 50 control women at age [29.1 +/- 6.8] were included in this study. Genotyping of INH alpha-16C>T gene was performed by restriction fragment length polymorphism. Levels of inhibin, activin, FSH and LH were also assessed


Results: Serum levels of FSH and LH showed significant increase coupled by decrease in serum inhibin and inhibin/activin ratio, however, levels of activin were within normal values in POF women comparing to control ones. The frequencies of CC, CT and TT genotypes showed no significant changes in POF women compared to control group. Moreover, there were no significant differences in frequency of C and T alleles among the POF women in comparison to controls


Conclusion: Obtained data indicated that -16C>T polymorphism of INH alpha gene can not imply a functional effect on the current decline of serum inhibin and hence the risk of developing POF in the studied Egyptian women. Further studies on POF women are needed to expand the present data


Subject(s)
Humans , Adult , Women , Inhibins/genetics , Inhibins/chemistry , Activins , Polymorphism, Genetic , Polymorphism, Restriction Fragment Length , Ovulation Induction , Genotyping Techniques , Polymerase Chain Reaction
2.
Femina ; 39(7): 351-356, jul. 2011.
Article in Portuguese | LILACS | ID: lil-613323

ABSTRACT

A endometriose é uma condição ginecológica, que atinge mulheres em idade reprodutiva e pode ser causa de dor e infertilidade. A patogênese da doença é multifatorial e envolve a perda da capacidade de diferenciação das células endometrióticas, moléculas de adesão celular para adesão do endométrio ao peritônio, neoangiogênese, características do fluido peritoneal e alterações do sistema imune. A superfamília do fator transformador de crescimento β (TGF-β) parece exercer papéis importantes na implantação e manutenção do tecido ectópico na endometriose. Ativinas, inibinas, folistatina, hormônio anti-mülleriano e as proteínas morfogenéticas ósseas são membros da superfamília do TGF-β. Estas moléculas são expressas no endométrio humano e apresentam ações importantes na proliferação celular, diferenciação celular, função imune, regulação da apoptose e remodelamento dos tecidos, apresentando, por conseguinte, um importante papel no ciclo menstrual, decidualização do endométrio e no início da gestação. Este artigo objetiva rever os achados sobre tais proteínas no endométrio e seus possíveis papéis na gênese e fisiopatologia da endometriose


Endometriosis is a gynecological pathological entity typical of women in reproductive age, associated with pelvic pain and infertility. The pathogenesis of the disease is multifactorial and it involves loss of the endometriotic cell differentiation, cell adhesion, neo-angiogenesis, peritoneal fluid characteristics, and changes in the immune system. The transforming growth factor β (TGF-β) superfamily seems to play important roles in the implementation and maintenance of ectopic tissue in endometriosis. Activin, inhibin, follistatin, anti-Mullerian hormone, and bone morphogenetic proteins are members of the superfamily of TGF-β. The TGF-β and family members are expressed by human endometrium and act on cell proliferation, differentiation, immune function, apoptosis and tissue remodeling, playing a role in menstrual cycle, decidualization, and early pregnancy. The aim of this study is to review the findings about these molecules in the endometrium and their possible roles in the genesis and pathophysiology of endometriosis


Subject(s)
Humans , Female , Activins/pharmacology , Activins/genetics , Endometrium/metabolism , Endometriosis/physiopathology , Endometriosis/metabolism , Transforming Growth Factor beta/physiology , Inhibins/pharmacology , Inhibins/genetics , Cell Differentiation , Menstrual Cycle/metabolism , Infertility, Female/etiology , Cell Proliferation
3.
Journal of Veterinary Science ; : 345-349, 2008.
Article in English | WPRIM | ID: wpr-146092

ABSTRACT

Inhibin, which is important for normal gonadal function, acts on the pituitary gonadotropins to suppress folliclestimulating hormone (FSH) secretion. The level and cellular localization of the inhibin isotypes, alpha, beta(A) and beta(B), in the testis of mice were examined during postnatal development in order to determine if inhibin expression is related to testicular maturation. Mouse testes were sampled on postnatal days (PNDs) 1, 3, 6, 18, 48 and 120, and analyzed by Western blotting and immunofluorescence. Western blot analysis showed very low levels of inhibin alpha, beta(A) and beta(B) expression in the testes at days 1 to 6 after birth. The levels then increased gradually from PND 18 to 48-120, and there were significant peaks at PND 48. Inhibin alpha, beta(A) and beta(B) were detected in testicular cells during postnatal development using immunohistochemistry. The immunoreactivity of inhibin alpha was rarely observed in testicular cells during PND 1 to 6, or in the cytoplasmic process of Sertoli cells surrounding the germ cells and interstitial cells during PND 18 to 120. Inhibin beta(A) and beta(B) immunoreactivity was rarely observed in the testis from PND 1 to 6. On the other hand, it was observed in some spermatogonial cells, as well as in the interstitial space between PND 48 and PND 120. We conclude that the expression of inhibin isotypes increases progressively in the testis of mice with increasing postnatal age, suggesting that inhibin is associated with a negative feedback signal for FSH in testicular maturation.


Subject(s)
Animals , Male , Mice , Aging/physiology , Gene Expression Regulation/physiology , Inhibin-beta Subunits/genetics , Inhibins/genetics , Mice, Inbred ICR , Protein Isoforms/metabolism , Protein Transport/physiology , Testis/metabolism
4.
Yonsei Medical Journal ; : 479-482, 2004.
Article in English | WPRIM | ID: wpr-14511

ABSTRACT

Premature ovarian failure (POF) is menopause before the age of 40 years. The frequency of POF is about 1% of all women. Recently inhibin alpha gene (INHalpha) has been indicated as candidate in POF pathogenesis. Inhibin, a glycoprotein, is a gonadal hormone, which can inhibit the synthesis and secretion of pituitary follicle-stimulating hormone (FSH), which has an important role in the recruitment and development of ovarian follicles during the folliculogenesis. G769A variation of INH alpha, alanine, is highly conserved across species, and has an important role of its receptor binding. We screened a G769A transition in the INHalpha from the total population of the patients of 84 women with POF and 100 normal fertile women. We found no variation between the normal subjects and the POF patients. G769A variation of INHalpha is rare in Korea women with POF.


Subject(s)
Adult , Female , Humans , Follicle Stimulating Hormone/metabolism , Infertility, Female/genetics , Inhibins/genetics , Korea , Primary Ovarian Insufficiency/genetics , Polymorphism, Restriction Fragment Length
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