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In-vitro evaluation of exocytosis-associated snaremolecules in granulosa cells in polycystic ovary syndrome

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2021
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Abstract (EN)

Polycystic ovary syndrome is the most common cause of chronic anovulation in women of reproductive age and may require assisted reproductive treatment. Dysregulation of intra-follicular growth factors and other signal molecules has been determined in studies for polycystic ovary syndrome. As a result of the disruption of the intra-follicular environment, folliculogenesis breaks down and oligo/anovulation occurs. The impairment of synthesis or exocytosis in the membrane granulosa cells may be responsible for dysregulation in the amount of intra-follicular signaling molecule. In this thesis, the expression level of Stx6, SNAP 25, and StxBP1 proteins, which are the vesicle fusion proteins, of granulosa cells in PCOS were investigated in comparison to healthy women. For this purpose, granulosa cells of follicle fluid were isolated who PCOS (n=10) and male factor (n=10) infertility patient, then immunofluorescence labeling method was used. Also, human granulosa cells were proliferated in-vitro then examined by electron microscopy for intracellular vesicles. It has been shown that Stx6, SNAP 25, and StxBP1 levels are decreased in PCOS. It was observed that the KITL secreted by granulosa cells decreased in the cell in the PCOS. Electron density of the vesicles decreased in granulosa cells. According to our results, granulosa cells in PCOS compared to healthy granulosa cells; it was demonstrated that the number of vesicles decreased, vesicular response to FSH-hCG stimulation was impaired, and Stx6, SNAP25, StxBP1 levels decreased. As a result, it has been revealed that there is a disruption in the secretion of granulosa cell-derived factors, which are impaired in PCOS, as well as in the synthesis.

Author

Süleyman Erol

How to Cite

Süleyman Erol (Medical Specialty Thesis). In-vitro evaluation of exocytosis-associated snaremolecules in granulosa cells in polycystic ovary syndrome, 2021, Hacettepe University.

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