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长链非编码RNA MEG8通过甲基化上调miR-770-5p并促进糖尿病肾病中的细胞凋亡。

lncRNA MEG8 Upregulates miR-770-5p Through Methylation and Promotes Cell Apoptosis in Diabetic Nephropathy.

作者信息

Zhang Jinmei, Song Liwen, Ma Yanjuan, Yin Yan, Liu Xinqi, Luo Xinyu, Sun Jiali, Wang Liqin

机构信息

Department of Endocrinology, Weifang Hospital of Traditional Chinese Medicine, Weifang, Shandong Province 261000, People's Republic of China.

Department of Endocrinology, Weifang People's Hospital, Weifang, Shandong Province 261000, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2020 Jul 10;13:2477-2483. doi: 10.2147/DMSO.S255183. eCollection 2020.

Abstract

BACKGROUND

It has been reported that lncRNA MEG8 can be induced by glucose in mice model of kidney injury, indicating its role in diabetic nephropathy (DN). This study was carried out to explore the role of MEG8 in DN.

MATERIALS AND METHODS

The expression of MEG8 and miR-770-5p in plasma samples from DN patients (n = 66), diabetic patients (DM patients with no complications, n = 66) and healthy controls (n = 66) was detected by RT-qPCR. The interaction between MEG8 and miR-770-5p in podocyte cells was evaluated by transient transfections. Cell apoptosis under high-glucose treatment was detected by cell apoptosis assay.

RESULTS

MEG8 and miR-770-5p were upregulated in plasma of DM patients and were further upregulated in DN patients. MEG8 was positively correlated with miR-770-5p. In podocyte cells, high-glucose treatment resulted in increased expression levels of MEG8 and miR-770-5p. In podocyte cells, overexpression of MEG8 resulted in upregulated expression of miR-770-5p and decreased methylation of the miR-770-5p gene. Cell apoptosis analysis showed that overexpression of MEG8 and miR-770-5p resulted in increased cell apoptotic rate under glucose treatment. In addition, combined overexpression of MEG8 and miR-770-5p showed stronger effects.

CONCLUSION

MEG8 may upregulate miR-770-5p through methylation to promote DN by promoting cell apoptosis.

摘要

背景

据报道,在肾脏损伤小鼠模型中,长链非编码RNA MEG8可被葡萄糖诱导,表明其在糖尿病肾病(DN)中发挥作用。本研究旨在探讨MEG8在DN中的作用。

材料与方法

采用逆转录定量聚合酶链反应(RT-qPCR)检测糖尿病肾病患者(n = 66)、糖尿病患者(无并发症的糖尿病患者,n = 66)和健康对照者(n = 66)血浆样本中MEG8和miR-770-5p的表达。通过瞬时转染评估足细胞中MEG8与miR-770-5p之间的相互作用。采用细胞凋亡检测法检测高糖处理下的细胞凋亡情况。

结果

糖尿病患者血浆中MEG8和miR-770-5p上调,糖尿病肾病患者中进一步上调。MEG8与miR-770-5p呈正相关。在足细胞中,高糖处理导致MEG8和miR-770-5p表达水平升高。在足细胞中,MEG8过表达导致miR-770-5p表达上调,miR-770-5p基因甲基化降低。细胞凋亡分析表明,MEG8和miR-770-5p过表达导致高糖处理下细胞凋亡率增加。此外,MEG8和miR-770-5p联合过表达显示出更强的作用。

结论

MEG8可能通过甲基化上调miR-770-5p,促进细胞凋亡从而促进糖尿病肾病的发生发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999c/7360416/9c7eb5faeeb4/DMSO-13-2477-g0001.jpg

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