Identification of several circulating microRNAs from a genome-wide circulating microRNA expression profile as potential biomarkers for impaired glucose metabolism in polycystic ovarian syndrome

Jiang, Linlin; Huang, Jia; Chen, Yaxiao; Yang, Yu-Chih; Li, Ruiqi; Yu, Lap-Fai; Chen, Xiaoli; Yang, Dongzi

doi:10.1007/s12020-016-0878-9

Cited by 60 publications

(42 citation statements)

References 47 publications

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“…51 Scholars also found that miR-199b-5p was downregulated in PCOS and predicted the involvement of the PI3K-Akt signaling pathway in disease pathophysiology. 56 Moreover, in the endometrial cells of patients with PCOS-IR, the change in the PI3K-Akt signaling pathway was found to affect IR. Rivero et al 57 used telomerase-immortalized human endometrial stromal cells (T-HESCs) from PCOS with IR and observed that when T-HESCs were stimulated with insulin and testosterone, the protein levels of Munc18c and phospho-PKCz decreased.…”

Section: The Pi3k-akt Signaling Pathway and Irmentioning

confidence: 96%

Role of the PI3K-Akt Signaling Pathway in the Pathogenesis of Polycystic Ovary Syndrome

et al. 2017

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This review aimed to focus on the recent progress of the understanding of the role of phosphatidylinositol 3-kinase (PI3K) in polycystic ovary syndrome (PCOS). In recent years, it has been increasingly recognized that PI3K plays an important role in PCOS whose pathogenesis is unclear. However, research continues into revealing the details of how PI3Ks are involved in developing PCOS. Previous studies have shown that activation of the PI3K-protein kinase B (Akt) signaling pathway has important effects on insulin resistance and endometrial cancer. Knowledge of the action of PI3K in PCOS might provide valuable information to further validate the pathogenesis of PCOS and suggest new methods of treatment.

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Section: The Pi3k-akt Signaling Pathway and Irmentioning

confidence: 96%

Role of the PI3K-Akt Signaling Pathway in the Pathogenesis of Polycystic Ovary Syndrome

et al. 2017

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“…A genome-wide circulating miRNA expression profile identified a number of miRNAs dysregulated in women with PCOS. These miRNA species are involved in glycometabolism and ovarian follicle development pathways [111, 112]. Interestingly, miRNA-592 has been shown to be downregulated and to be inversely related to LHCGR levels in PCOS patients [113].…”

Section: A Pathophysiologymentioning

confidence: 99%

An International Consortium Update: Pathophysiology, Diagnosis, and Treatment of Polycystic Ovarian Syndrome in Adolescence

Ibáñez¹,

et al. 2017

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This paper represents an international collaboration of paediatric endocrine and other societies (listed in the Appendix) under the International Consortium of Paediatric Endocrinology (ICPE) aiming to improve worldwide care of adolescent girls with polycystic ovary syndrome (PCOS)¹. The manuscript examines pathophysiology and guidelines for the diagnosis and management of PCOS during adolescence. The complex pathophysiology of PCOS involves the interaction of genetic and epigenetic changes, primary ovarian abnormalities, neuroendocrine alterations, and endocrine and metabolic modifiers such as anti-Müllerian hormone, hyperinsulinemia, insulin resistance, adiposity, and adiponectin levels. Appropriate diagnosis of adolescent PCOS should include adequate and careful evaluation of symptoms, such as hirsutism, severe acne, and menstrual irregularities 2 years beyond menarche, and elevated androgen levels. Polycystic ovarian morphology on ultrasound without hyperandrogenism or menstrual irregularities should not be used to diagnose adolescent PCOS. Hyperinsulinemia, insulin resistance, and obesity may be present in adolescents with PCOS, but are not considered to be diagnostic criteria. Treatment of adolescent PCOS should include lifestyle intervention, local therapies, and medications. Insulin sensitizers like metformin and oral contraceptive pills provide short-term benefits on PCOS symptoms. There are limited data on anti-androgens and combined therapies showing additive/synergistic actions for adolescents. Reproductive aspects and transition should be taken into account when managing adolescents.

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“…MicroRNAs (miRNAs, miRs) are evolutionarily conserved small noncoding RNA molecules that function as negative post-transcriptional gene regulators [ 6 ]. Because of the ability of a single miRNA molecule to target hundreds of messenger RNAs (mRNAs), abnormal miRNA expression is associated with the initiation of many diseases [ 7 ]. Recent studies have suggested that miRNAs may be involved in the development of GA [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-488 and -920 regulate the production of proinflammatory cytokines in acute gouty arthritis

Zhou

Wang

et al. 2017

Arthritis Res Ther

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BackgroundGout is considered one of the most painful acute conditions caused by deposition of monosodium urate (MSU) crystals within joints. Recent studies have shown that interleukin (IL)-1β is a key inflammatory mediator in acute gouty arthritis (GA), and its level is regulated by microRNAs (miRNAs). However, the molecular mechanisms of the regulation remain unclear.MethodsA miRNA microarray was used to analyze the miRNA expression profiles in peripheral white blood cells (WBCs) of patients with GA. THP-1 cells were transfected with miRNA mimics, stimulated by MSU crystals, and then subjected to quantitative real-time polymerase chain reaction or Western blot analysis. Levels of IL-1β, IL-8, and tumor necrosis factor (TNF)-α in culture supernatants of THP-1 cells were measured by enzyme-linked immunosorbent assay. A luciferase reporter assay was conducted to confirm the interaction of miRNA and IL-1β 3′-untranslated regions (UTRs).ResultsCombining bioinformatics and miRNA expression profiles, we found five miRNAs (hsa-miR-30c-1-3p, hsa-miR-488-3p, hsa-miR-550a-3p, hsa-miR-663a, and hsa-miR-920) that possibly target IL-1β. Then, we demonstrated that miR-488 and miR-920 were significantly decreased in the WBCs of patients with GA and that MSU crystals could inhibit expression of miR-488 and miR-920. Upregulation of miR-488 and miR-920 could suppress MSU-induced IL-1β protein expression in THP-1 cells, but no significant difference in IL-1β messenger RNA levels was observed. Moreover, we found that miR-488 and miR-920 could directly target the 3′-UTR of IL-1β. Overexpression of miR-488 and miR-920 could significantly inhibit the gene and protein expression of IL-8 and TNF-α in MSU-induced THP-1 cells.ConclusionsThis study demonstrates the roles of miR-488 and miR-920 in regulating the production of proinflammatory cytokines in the pathogenesis of GA. These findings suggest that miR-488 and miR-920 could serve as potential therapeutic targets in the treatment of GA.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-017-1418-6) contains supplementary material, which is available to authorized users.

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Identification of several circulating microRNAs from a genome-wide circulating microRNA expression profile as potential biomarkers for impaired glucose metabolism in polycystic ovarian syndrome

Cited by 60 publications

References 47 publications

Role of the PI3K-Akt Signaling Pathway in the Pathogenesis of Polycystic Ovary Syndrome

Role of the PI3K-Akt Signaling Pathway in the Pathogenesis of Polycystic Ovary Syndrome

An International Consortium Update: Pathophysiology, Diagnosis, and Treatment of Polycystic Ovarian Syndrome in Adolescence

MicroRNA-488 and -920 regulate the production of proinflammatory cytokines in acute gouty arthritis

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