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长链非编码RNA SNHG4通过吸附miR-200b抑制糖尿病视网膜病变中的细胞凋亡。

LncRNA SNHG4 sponges miR-200b to inhibit cell apoptosis in diabetic retinopathy.

作者信息

Yu Jia, Qin Mei, Li Juan, Cui Shumin

机构信息

Department of Ophthalmology, The First Affiliated Hospital of Bengbu Medical College, Bengbu City, People's Republic of China.

出版信息

Arch Physiol Biochem. 2023 Oct;129(5):1117-1122. doi: 10.1080/13813455.2021.1900873. Epub 2021 Apr 6.

DOI:10.1080/13813455.2021.1900873
PMID:33822671
Abstract

This study aimed to investigate the role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 4 (SNHG4) in diabetic retinopathy (DR). We found that SNHG4 was downregulated in DR. SNHG4 could directly interact with miR-200b, while overexpression of miR-200b did not affect the expression of SNHG4 in human retinal pigment epithelial cells ARPE-19. In contrast, overexpression of SNHG4 led to the upregulation of oxidation resistance 1 (Oxr1), a target of miR-200b. Cell apoptosis analysis showed that overexpression of miR-200b increased the apoptotic rate of ARPE-19 cells under high glucose treatment. Oxr1 and SNHG4 played opposite roles and reduced the effects of overexpression of miR-200b. In conclusion, SNHG4 may sponge miR-200b to inhibit cell apoptosis in DR by upregulating Oxr1.

摘要

本研究旨在探讨长链非编码RNA(lncRNA)小核仁RNA宿主基因4(SNHG4)在糖尿病视网膜病变(DR)中的作用。我们发现SNHG4在DR中表达下调。SNHG4可直接与miR-200b相互作用,而miR-200b的过表达并不影响人视网膜色素上皮细胞ARPE-19中SNHG4的表达。相反,SNHG4的过表达导致miR-200b的靶标抗氧化1(Oxr1)上调。细胞凋亡分析表明,miR-200b的过表达增加了高糖处理下ARPE-19细胞的凋亡率。Oxr1和SNHG4发挥相反作用,并减弱了miR-200b过表达的影响。总之,SNHG4可能通过上调Oxr1来吸附miR-200b,从而抑制DR中的细胞凋亡。

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