A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Functional Characterization of MicroRNA-27a-3p Expression in Human Polycystic Ovary Syndrome
Tekijät: Mingming Wang, Jing Sun, Bo Xu, Marcin Chrusciel, Jun Gao, Maciei Bazert, Joanna Stelmaszewska, Yunyun Xu, Hongwen Zhang, Leszek Pawelczyk, Fei Sun, Suk Ying Tsang, Nafis Rahman, Sławomir Wołczyński, Xiangdong Li
Kustantaja: American Endocrine Society
Julkaisuvuosi: 2018
Journal: Endocrinology
Tietokannassa oleva lehden nimi: Endocrinology
Lehden akronyymi: Endocrinology
Vuosikerta: 159
Numero: 1
Aloitussivu: 297
Lopetussivu: 309
Sivujen määrä: 13
ISSN: 1945-7170
DOI: https://doi.org/10.1210/en.2017-00219
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/28557129
The goal of this study was to characterize the function of microRNA-27a-3p (miR-27a-3p) in polycystic ovary syndrome (PCOS). miR-27a-3p expression was analyzed in excised granulosa cells (GCs) from 21 patients with PCOS and 12 normal patients undergoing in vitro fertilization cycle treatments and in 17 nontreated cuneiform ovarian resection PCOS samples and 13 control ovarian samples from patients without PCOS. We found that the expression of miR-27a-3p was significantly increased in both excised GCs and the ovaries of patients with PCOS compared with the controls. Insulin treatment of the human granulosa-like tumor cell line (KGN) resulted in decreased downregulated expression of miR-27a-3p, and this effect appeared to be mediated by signal transducer and activator of transcription STAT1 and STAT3. The overexpression of miR-27a-3p in KGN cells inhibited SMAD5, which in turn decreased cell proliferation and promoted cell apoptosis. After KGN cells were stimulated with insulin for 48 hours, there was increased expression of SMAD5 protein and decreased apoptosis. Additionally, knockdown/overexpression of SMAD5 in KGN cells reduced/increased cell number and promoted/inhibited cell apoptosis. Insulin-stimulated primary GCs isolated from patients with PCOS, in contrast to normal GCs or KGN cells, did not exhibit decreased miR-27a-3p expression. The differences in the expression levels in KGN cells and human PCOS GCs are likely explained by increased miR-27a-3p expression in the GCs caused by insulin resistance in PCOS. Taken together, our data provided evidence for a functional role of miR-27a-3p in the GCs' dysfunction that occurs in patients with PCOS.
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