Dissertation > Medicine, health > Obstetrics and Gynaecology > Gynecology > Other diseases of the female genital > Ovarian disease

The Research on Relationship between Leptin Postreceptor Signal Transduction Molecular STAT3 Phosphorylation in Ovarain Luteinizated Granulosa Cells and Mechanism of Polycystic Ovarian Syndrome

Author YinZuo
Tutor LiuYi
School Huazhong University of Science and Technology
Course Obstetrics and Gynaecology
Keywords Polycystic ovary syndrome Granulosa cells Leptin Leptin receptor Leptin signal transduction p-STAT3
CLC R711.75
Type Master's thesis
Year 2007
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Objective: Clinical observation of about 50% of women with polycystic ovary syndrome (Polycystic ovarian syndrome, PCOS) patients with obesity, and the majority of patients with PCOS weight gradually increased after the onset of symptoms, to further the cause of women in the reproductive endocrine disorders. Leptin can directly inhibit IGF-1 ovarian granulosa cells, thereby inhibiting granulosa cell differentiation and oocyte maturation, blocking the dominant follicle choice and follicular development, and lead to ovulation. However, the exact mechanism is not yet clear. JAK2-STAT3 pathway is now considered the leptin signal transduction pathway, the major route through the leptin long receptor activation. Of this study is to determine the obese and non-obese PCOS patients with ovarian Huang Suhua granulosa cell surface leptin long receptor mRNA (OB-RLmRNA) of intracellular signal transduction molecules STAT3 phosphorylation (p-STAT3) levels, leptin in in the pathogenesis of PCOS. At the same time, the experiment also observed different concentrations of leptin on cultured normal population luteinized the granulosa cells the OB-RLmRNA and the impact of p-STAT3, to explore the relationship between the OB-RLmRNA and p-STAT3 and leptin and PCOS. Methods: in vitro fertilization - embryo transfer (IVF-ET) treatment of obese patients with PCOS (obese PCOS group), non-obese PCOS patients (non-obese PCOS group), with normal ovulatory function and simple tubal factor infertility obesity ( the normal obese group) and normal weight women (the control group) 10 cases, specimens from follicular fluid recycling egg precipitation luteinized granulosa cells. By semi-quantitative RT-PCR and Western blot (Western blot) p-STAT3 levels of The detection luteinizing granulosa cells of OB-RLmRNA the expression and leptin signal transduction molecules. Another the same period in the normal control group human luteinized granulosa cells cultured and treated with different concentrations of leptin (0,10,100,1000 ng / ml) to stimulate 48h, were measured under various concentrations of leptin stimulate human ovarian luteinizing granulosa The cells surface OB-RLmRNA of the expression level of p-STAT3. Results: (1) RT-PCR results show that the normal control group, the the normal obese group, the non-obese PCOS and obese PCOS group luteinized granulosa cells leptin expression levels of OB-RLmRNA in turn increased the expression differences between groups was statistically significant (p lt; 0.05). (2) The obese PCOS group, normal obese group, non-obese PCOS group and normal control group ovarian luteinized of particles cell p--of STAT3 level were (24.28 ± 0.51), (21.31 ± 1.32), (11.69 ± 0.67), (9.03 ± 0.20), each group difference was statistically significant (p lt; 0.05), which obese PCOS group luteinized granulosa cells of the highest levels of p-STAT3 expression; (3) leptin in vitro ovarian luteinizing granulosa cells can significantly promote the OB-RLmRNA , OB-RLmRNA highest expression levels of p-STAT3 and p-STAT3 expression (P lt; 0.01), and a dose-dependent manner, when the when leptin concentration reaches 100ng/ml. Conclusions: (1) serum leptin levels in obese PCOS by promoting ovarian granulosa cells leptin the OB-RLmRNA and the expression of p-STAT3 cause granulosa cells may be involved in the increased sensitivity to leptin response, obesity, type PCOS anovulatory occurrence; (2) JAK2/STAT3 signaling pathway may be involved in the role of leptin in PCOS anovulatory.

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