LncRNA HOTAIR up-regulates the expression of IGF1 and aggravates the endocrine disorders and granulosa cell apoptosis through competitive binding to miR-130a in rat models of PCOS.
In conclusion, miR-323-3p targeting IGF-1 regulates the steroidogenesis and the activity of CCs, which plays an important role in the occurrence and development of PCOS.
Real-time PCR arrays indicated that 7 and 34 autophagy-related genes were down- and up-regulated in human PCOS , Signal-Net, and regression analysis suggested that there are a wide range of interactions among these 41 genes, and a potential network based on <i>EGFR, ERBB2, FOXO1, MAPK1, NFKB1, IGF1,</i><i>TP53</i> and <i>MAPK9</i> may be responsible for autophagy activation in PCOS.
Luciferase assay, reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to determine whether IGF‑1 was a target of miR‑19b. miR‑19b expression was significantly decreased in the PCOS ovarian cortex and KGN cells and its identified target, IGF‑1, was upregulated. miR‑19b overexpression inhibited cell proliferation at G2/M phrase.
Knockdown of klotho gene expression normalized IGF-1R and Wnt1 protein expressions and Akt phosphorylation in GCs from patients with PCOS and the ovarian tissues from PCOS rats; it also blocked the effects of insulin on apoptosis and proliferation in GCs from patients with PCOS and inhibited caspase-3 activity in ovarian tissues of PCOS rats.
Cooperative effects of androgen and IGF-I counteract endogenous BMP-6 activity in rat granulosa cells, which is likely to be functionally linked to the steroidogenic property shown in the PCOS ovary.
Expression of IGF-1 and LEPR indicates a relevant role in androgenic features reversion present in PCOS, hormonal equilibrium, body weight regulation, and glucose metabolism, therefore, under phenotype obesity and infertility regulation in this model.
To test the hypothesis that insulin signalling plays a key role in the development of EC in women with PCOS by measuring and comparing the expression of three key genes involved in the insulin signalling pathway (IGF1, PTEN and IGFBP1) in endometrial tissue obtained from three groups of women; PCOS without EC, women with EC without PCOS and non-PCOS women without EC (controls).
IGF-1 stimulated initiation of follicle growth in normal tissue but had little effect on preantral follicle growth in polycystic ovaries in which, characteristically, there was a higher proportion of follicles that had entered the growing phase even before culture.
The hypothesis that high concentrations of IGF1 can impair embryo development was investigated in a bovine in vitro model to reflect conditions in polycystic ovary syndrome (PCOS) patients.
Gene expression for IGF-binding protein (IGFBP) 3 in GCs definitely differed between normal women and women with PCOS, whereas increase in IGF-I and IGF receptor (IGFR) 2 mRNA in mature-follicle GCs, increase in IGF-II, IGFR-1, and IGFBP-4 mRNA in immature-follicle GCs, increase in IGFR-2 and IGFBP-2 mRNA in mature-follicle CCs, and increase IGFBP-6 mRNA in immature-follicle CCs were observed in both normal women and women with PCOS.
Our objective was to assess the induction of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) expression with insulin treatment and effects of PTEN on IGF-I-induced granulosa cell proliferation as well as the correlation of PTEN levels with the concentration of insulin in follicular fluid in PCOS and non-PCOS patients.
PCOS patients whose IGF-I levels decreased from day 3 to day of hCG had a significantly higher mean number of immature oocytes retrieved (4.8 +/- 1.1 vs. 2.4 +/- 0.4; P=.02).
Troglitazone increased the insulin-induced glycogen synthesis but reduced the IGF-1-augmented responses of DNA synthesis in PCOS cells to the range within those of NO granulosa cells.
Plasma IGF-1 levels are higher in cases of severe endometriosis, however, in endometriosis and in PCOIGF levels locally in the endometrium are reduced, what might explain infertility.