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Anti-Mullerian Hormone Induces Foxo1 and Sirt1 Genes Expression in Mouse Ovary
被引:0
|作者:
Abouzeid, Hoda M.
[1
]
Hashad, Ingy M.
[1
]
Rady, Mona
[2
,3
]
Abdel-Maksoud, Sahar M.
[1
]
机构:
[1] German Univ Cairo, Fac Pharm & Biotechnol, Biochem Dept, Cairo, Egypt
[2] German Univ Cairo, Fac Pharm & Biotechnol, Microbiol Immunol & Biotechnol Dept, Cairo, Egypt
[3] German Int Univ, Fac Biotechnol, New Adm Capital, New Cairo, Egypt
关键词:
Anti-Mullerian hormone (AMH);
Atresia;
Foxo1;
Polycystic ovary syndrome (PCOS);
Sirt1;
p53;
Bim;
and Bax;
FORKHEAD TRANSCRIPTION FACTORS;
GRANULOSA-CELL APOPTOSIS;
FOLLICULAR ATRESIA;
AMH;
FSH;
REGULATOR;
DEPLETION;
DEATH;
CYCLE;
PCOS;
D O I:
10.2174/0113892010293250240917143811
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Background: Anti-Mullerian hormone (AMH) plays a pivotal role in follicular growth and atresia. Recent studies highlighted the role of AMH in attenuating granulosa cell apoptosis and subsequent follicular atresia. Despite the raising understanding of the role of AMH in folliculogenesis, and its contribution to the pathophysiology of certain diseases such as polycystic ovary syndrome, the effect of AMH on the expression of genes regulating folliculogenesis is stills limited. Objective: This study aims to gain insights into the effect of AMH on atresia regulating genes. Method In vivo study was performed on C57BL/6J mice injected with AMH for one month. Thereafter, relative gene expression quantification of Foxo1, Sirt1, p53, Bim, and Bax genes were performed using RT-PCR. Results: In this study, AMH significantly enhanced the expression of Foxo1 and Sirt1 gene compared to the control group. On the contrary, AMH did not modulate the expression of p53, Bim, or Bax genes. AMH was also found to increase serum FSH and LH levels in a dose-dependent manner. Conclusion: This study demonstrated the capability of AMH to induce Foxo1 and Sirt1 genes. Moreover, our study revealed the role of AMH in elevating LH serum level which is a main contributor to the pathophysiology of polycystic ovary syndrome, opening new avenues for the study of AMH as a main contributor to the stalled follicular atresia and growth associated with the disease.
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