MicroRNA expression profiling in the adult offspring of rats with periodontal disease

IF 2.2 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology Pub Date : 2024-11-14 DOI:10.1016/j.archoralbio.2024.106131

Maria Sara de Lima Coutinho Mattera , Natália Francisco Scaramele , Flávia Lombardi Lopes , Bianca Elvira Belardi , Thaís Verônica Saori Tsosura , Heloisa Macedo Sampaio , Fernando Yamamoto Chiba , Renato Felipe Pereira , Rodrigo Martins dos Santos , Edilson Ervolino , Gabriele Fernandes Baliero , Ana Carla Thalez Ywabuchi Nobumoto , Anna Clara Cachoni , Antonio Hernandes Chaves-Neto , Doris Hissako Matsushita

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引用次数: 0

Abstract

Objective

The present study investigated the relationship between maternal periodontal disease, insulin resistance, activation of inflammatory pathways and epigenetic modifications in adult offspring.

Design

Therefore, female Wistar rats were divided into control and experimental groups. Seven days after the induction of periodontal disease, female rats from both groups were mated with healthy male rats. After weaning, male offspring were divided into control offspring (CN-o) and periodontal disease offspring (PED-o) groups. Body weight was measured at 0–75 days of age. At day 75, the following were measured in the offspring: insulin resistance by the HOMA-IR index; global miRNAs by microtranscriptome array; validation of the selected miRNAs by quantitative real-time PCR expression; interleukin 1 receptor associated kinase 1 (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6) content in the gastrocnemius muscle tissue (GSM) by western blotting.

Results

Maternal periodontal disease leads to low birth weight (LBW) in the offspring and insulin resistance in adulthood; changes in global miRNA expression (5 miRNAs upregulated and 6 downregulated); and increased protein expression of IRAK1 and TRAF6 in GSM.

Conclusions

These findings demonstrate that maternal periodontal disease causes LBW, insulin resistance, activation of inflammatory pathways, and changes in global miRNA expression.

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牙周病大鼠成年后代的微RNA表达谱分析。

目的：本研究探讨了母体牙周病、胰岛素抵抗、炎症通路激活和成年后代表观遗传修饰之间的关系：本研究探讨了母体牙周病、胰岛素抵抗、炎症通路激活和成年后代表观遗传修饰之间的关系：设计：将雌性 Wistar 大鼠分为对照组和实验组。因此，雌性 Wistar 大鼠被分为对照组和实验组。在诱导牙周病七天后，两组雌性大鼠均与健康雄性大鼠交配。断奶后，将雄性后代分为对照后代组（CN-o）和牙周病后代组（PED-o）。在 0-75 日龄时测量体重。第 75 天时，对后代的以下指标进行了测量：HOMA-IR 指数显示的胰岛素抵抗；微转录组阵列显示的全球 miRNAs；实时定量 PCR 表达对所选 miRNAs 的验证；Western 印迹法显示的腓肠肌组织（GSM）中白细胞介素 1 受体相关激酶 1（IRAK1）和肿瘤坏死因子受体相关因子 6（TRAF6）的含量：结果：母体牙周病导致后代出生体重低（LBW）和成年后胰岛素抵抗；全球 miRNA 表达发生变化（5 个 miRNA 上调，6 个下调）；腓肠肌组织中 IRAK1 和 TRAF6 蛋白表达增加：这些研究结果表明，母体牙周病会导致婴儿畸形、胰岛素抵抗、炎症通路激活和全球 miRNA 表达的变化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of oral biology 医学-牙科与口腔外科

CiteScore

5.10

自引率

3.30%

发文量

177

审稿时长

26 days

期刊介绍： Archives of Oral Biology is an international journal which aims to publish papers of the highest scientific quality in the oral and craniofacial sciences. The journal is particularly interested in research which advances knowledge in the mechanisms of craniofacial development and disease, including: Cell and molecular biology Molecular genetics Immunology Pathogenesis Cellular microbiology Embryology Syndromology Forensic dentistry