Up-regulation of MiR-21 and 146a Expression and Increased DNA Damage Frequency in a Mouse Model of Polycystic Ovary Syndrome (PCOS)

Overview

Journal Bioimpacts

Specialty Biomedical Engineering

Date 2016 Aug 16

PMID 27525225

Citations 5

Authors

Mohammad Salimi-Asl

Hossein Mozdarani

Mehdi Kadivar

Affiliations

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Abstract

Introduction: Polycystic ovary syndrome (PCOS), a multigenic endocrine disorder, is highly associated with low-grade chronic inflammation, however its etiology remains unclear. In this study, we employed dehydroepiandrosterone (DHEA)-treated mice to reveal the molecular mechanism of inflammation and its correlation with oxidative stress in PCOS patients.

Methods: miR-21 and miR-146a expression levels were measured using quantitative real-time polymerase chain reaction (qRT-PCR). DNA strand breakage frequency was measured using the single cell gel electrophoresis (SCGE) assay (comet assay) and micronucleus test (MN). CRP levels were measured by ELISA method and ESR values were measured by means of Micro-Dispette (Fisher No: 02-675-256) tubes according to the manufacturer's instructions. Data were analyzed using one-way ANOVA in SPSS 21.0 software.

Results: Our results showed that miR-21 and miR-146a as inflammation markers were upregulated in the sample group in comparison with control group. Erythrocyte sedimentation rate (ESR) and C- reactive protein (CRP) levels were also increased in mouse models of PCOS (p < 0.000). Micronucleated polychromatic erythrocyte (MNPCE) rates per 1000 polychromatic erythrocyte (PCE) significantly increased in DHEA treated mice (6.22 ± 3.28) in comparison with the controls (2.33 ± 2.23, p < 0.000). Moreover, mean arbitrary unit in DHEA treated animals (277 ± 92) was significantly higher than that in controls (184 ± 76, p = 0.005).

Conclusion: To conclude, increased DNA strand breakage frequency and increased expression levels of miR-21 and miR-146a in DHEA administrated animals suggest that low grade chronic inflammation and oxidative stress can act as the main etiologies of PCOS.

Citing Articles

CIRCULATING MIR-132, MIR-146A, MIR-222, AND MIR-320 EXPRESSION IN DIFFERENTIAL DIAGNOSIS OF WOMEN WITH POLYCYSTIC OVARY SYNDROME.

Soyman Z, Durmus S, Ates S, Simsek G, Sozer V, Kundaktepe B Acta Endocrinol (Buchar). 2022; 18(1):13-19.

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MicroRNA-125b controls growth of ovarian granulosa cells in polycystic ovarian syndrome by modulating cyclin B1 expression.

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Increased miR-188-3p in Ovarian Granulosa Cells of Patients with Polycystic Ovary Syndrome.

Dai B, Jiang J Comput Math Methods Med. 2021; 2021:5587412.

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MicroRNA-9119 regulates cell viability of granulosa cells in polycystic ovarian syndrome via mediating Dicer expression.

Ding Y, He P, Li Z Mol Cell Biochem. 2020; 465(1-2):187-197.

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Impaired receptivity and decidualization in DHEA-induced PCOS mice.

Li S, Song Z, Song M, Qin J, Zhao M, Yang Z Sci Rep. 2016; 6:38134.

PMID: 27924832 PMC: 5141439. DOI: 10.1038/srep38134.

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