Key result
Ovarian VEGF inhibition in a DHEA-induced PCOS rat model partially restored the accumulation of small follicles and reduced cyst formation, improving ovulation and follicular development.
Why the study?
Does ovarian VEGF inhibition improve follicular development and reduce cyst formation in a rat model of DHEA-induced PCOS?
Does ovarian VEGF inhibition improve follicular development and reduce cyst formation in a rat model of DHEA-induced PCOS?
Answers are grounded in this paper and cite their sources.
Ovarian VEGF inhibition partially restores the accumulation of small follicles and reduces cyst formation in a DHEA-induced PCOS rat model, suggesting a potential therapeutic strategy to restore ovarian function.
Polycystic ovary syndrome (PCOS) is the most common endocrinological pathology among women of reproductive age. It is characterized by anovulation, oligo- or amenorrhea, hyperandrogenism, obesity, and insulin resistance. PCOS patients present with elevated levels of vascular endothelial growth factor (VEGF) in serum and follicular fluid. In this study, we examined the ovarian expression of angiopoietins (ANGPT) and their receptor tyrosine kinase receptor (TIE2), involved in the stabilization of blood vessels, in a rat model of dehydroepiandrosterone-induced PCOS. We also analyzed the effect of ovarian VEGF inhibition on ANGPT/TIE2, follicular development, and vascular stability. VEGF levels were increased in the PCOS ovaries, whereas the levels of its receptor fetal liver kinase-1 were decreased. In addition, the periendothelial cell area and the ANGPT1 to ANGPT2 ratio in the ovary were increased in the PCOS group. Percentage of primary follicles was increased and the percentage of preantral follicles and corpora lutea was decreased in the PCOS group. VEGF inhibition decreased the percentage of primary follicles close to control values. Interestingly, despite the presence of cysts in the ovaries from VEGF inhibitor-treated PCOS rats, its percentage was lower than the PCOS group without treatment. In summary, this study describes an alteration not only in the VEGF/fetal liver kinase-1 system but also in the ANGPT/TIE2 system in a dehydroepiandrosterone-induced PCOS rat model. This leads to an increase in periendothelial cell recruitment. We also demonstrated that ovarian VEGF inhibition can partially restore the accumulation of small follicles in PCOS rats and reduces cyst formation, improving ovulation and follicular development. Therefore, the inhibition of VEGF could be considered, in addition to other currently applied treatments, as a new strategy to be studied in PCOS patients to restore ovarian function.
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Abramovich et al. (2012) studied Polycystic ovary syndrome (PCOS). Ovarian VEGF inhibition vs. PCOS group without treatment / control was evaluated on Ovarian expression of ANGPT/TIE2, follicular development, and vascular stability. Ovarian VEGF inhibition in a DHEA-induced PCOS rat model partially restored the accumulation of small follicles and reduced cyst formation, improving ovulation and follicular development.
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