miRNA Profiling Reveals miRNA-130b-3p Mediates DENND1A Variant 2 Expression and Androgen Biosynthesis.

摘要: Polycystic ovary syndrome (PCOS) is a common endocrine disorder of reproductive-age women involving overproduction ovarian androgens and, in some cases, from the adrenal cortex. Family studies have established that PCOS complex heritable with genetic and epigenetic components. Several small, noncoding RNAs (miRNAs) been shown to be differentially expressed cells follicular fluid circulation PCOS. However, there are no reports global miRNA expression target gene analyses theca isolated normal cycling PCOS, which key elucidation basis for hyperandrogenemia characteristic With use small RNA deep sequencing (miR-seq), we identified 18 miRNAs cells; these, miR-130b-3p was predicted one genome-wide association study candidates, neoplastic vs domain containing 1A (DENND1A). We previously reported DENND1A variant 2 (DENND1A.V2), truncated isoform DENND1A, upregulated mediates augmented androgen biosynthesis cells. The comparison demonstrated decreased cells, correlated increased DENND1A.V2, cytochrome P450 17α-hydroxylase (CYP17A1) mRNA biosynthesis. mimic miR130b-3p DENND1A.V2 CYP17A1 expression. Thus, addition factors, post-transcriptional regulatory mechanisms via underly excess Ingenuity® Pathway Analysis Core Network Analyses suggest network by miR-130b-3p, luteinizing hormone/choriogonadotropin receptor, Ras-related protein 5B, signaling pathways they potentially may mediate hyperandrogenism