Polycystic ovary síndrome (PCOS) is a complex endocrine disorder that affects 5-10% of women in reproductive age. PCOS is considered as a multifactorial pathology with both genetic, and metabolic abnrmalities, including insulin and leptin resistance. We have previously found that granulosa from PCOS women has leptin resistance and decreased expression of aromatase. Altered miRNAs expression have been associated with diabetes, insulin resistance and inflammation. Different studies have found differential amounts of miRNA in blood, folicular fluid and granulosa in PCOS patients. Therefore, in the present work we aimed to study the expression of several miRNA previously found to be related with insulin resistance or estrogen synthesis.
âranulosa cells from control (20) and polycystic ovary syndrome women (20) were obtained as waste product from in vitro fecundation, after informed consent. The Project was approved by the local IRB. Total RNA was isolated, miRNA retrotranscribed, and quantified by qPCR.. Statistical significance was assessed by analysis of the variance followd by Bonferroni´s post hoc test. P value < 0.05 was considered to be statistically significant
Most miRNA expression determined in granulosa from PCOS women was not statistically different compared with granulosa from control donors. However, miRNA107 expression (a miRNA that negatively regulates proliferation) was significantly decreased in granulosa from PCOS women compared with granulosa from control donors, and it could mediate the proliferation of the follicles. On the other hand, miRNA320a expression was found significantly increased in granulosa from women with PCOS. Leptin or insulin stimulation of control granulosa cells produced an increase in miRNA107 expression, and a decrease in the expression of miRNA-320a
The expression of several miRNA is altered in PCOS, decreased miRNA107 may not induce insulin resistance but may promote proliferation, mediating the increased number of follicles; whereas the increased miRNA320a expression in granulosa from PCOS could mediate the insulin and leptin resistance that occurs in this syndrome.
Victor Sánchez-Margalet, M. Pinto-López, T. Vilariño-García, A. Pérez-Alonso, E. Santamaría-López, N. Prados, M. Fernández-Sánchez, L. Aguilera, P. Sánchez-Martín, M. Dorado and A. Pérez-Pérez
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