Key result
HOTAIR down-regulation alleviates endocrine disorders and granulosa cell apoptosis in PCOS rats by reducing IGF1.
Why the study?
The role of the HOTAIR/miR-130a/IGF1 axis in endocrine disorders and granulosa cell behavior in polycystic ovary syndrome rat models was unclear.
Does modulation of lncRNA HOTAIR affect endocrine disorders and granulosa cell apoptosis in rat models of PCOS?
Does modulation of lncRNA HOTAIR affect endocrine disorders and granulosa cell apoptosis in rat models of PCOS?
Down-regulation of lncRNA HOTAIR alleviates endocrine disorders and granulosa cell apoptosis in PCOS rat models by reducing IGF1 expression via miR-130a.
Answers are grounded in this paper and cite their sources.
May implicate HOTAIR/miR-130a/IGF1 axis in PCOS granulosa dysfunction; hypothesis-generating and requires human validation before any clinical consideration.
It has been found that long noncoding RNA HOTAIR, microRNA‐130a (miR‐130a) and insulin‐like growth factor 1 (IGF1) expression are associated with ovarian cancer, thus, we hypothesised that the HOTAIR/miR‐130a/IGF1 axis might associate with endocrine disorders and biological behaviours of ovarian granulosa cells in rat models of polycystic ovary syndrome (PCOS). PCOS rat models were established by injection of dehydro‐isoandrosterone, followed by treatment of si‐HOTAIR, oe‐HOTAIR, miR‐130a mimics or miR‐130a inhibitors. Serum hormonal levels were determined to evaluate endocrine conditions. The effect of HOTAIR and miR‐130a on activities of isolated ovarian granulosa cells was assessed, as well as the involvement of IGF1.In the ovarian tissues and granulosa cells of PCOS rat models, highly expressed HOTAIR and IGF1 and poorly expressed miR‐130a were identified. In response to oe‐HOTAIR, serum levels of E 2 , T and LH were increased and serum levels of FSH were reduced; the proliferation of granulosa cells was reduced and apoptosis was promoted; notably, expression of miR‐130a was reduced while expression of IGF1 was increased. The treatment of si‐HOTAIR reversed the situation. Furthermore, the binding of HOTAIR to miR‐130a and targeting relationship of miR‐130a and IGF1 were confirmed. 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. Based on our finding, we predict that competitive binding of HOTAIR to miR‐130a may act as a novel target for the molecular treatment of PCOS.
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Jiang et al. (2019) studied Polycystic ovary syndrome (PCOS). si-HOTAIR, oe-HOTAIR, miR-130a mimics or miR-130a inhibitors was evaluated on Serum hormonal levels and granulosa cell proliferation and apoptosis. Down-regulation of lncRNA HOTAIR alleviated endocrine disorders and granulosa cell apoptosis in PCOS rat models by reducing IGF1 expression via competitive binding to miR-130a.
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