Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats.
Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats.
复制标题
Vof16-miR-205-Gnb3轴调节认知障碍糖尿病大鼠海马神经元功能
DOI：
10.21037/atm-21-2016
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发表时间：
2021-06
影响因子：
--
通讯作者：
Huang S
中科院分区：
文献类型：
--
作者：
Peng W;Xu B;Ge X;Du J;Xi L;Xia L;Wang Q;Huang S
背景糖尿病是一种慢性代谢性疾病，是认知功能损害的独立危险因素。非蛋白质编码RNA，包括长链非编码RNA（lncRNA）和微小RNA（miRNAs），参与各种病理生理条件。方法采用链脲佐菌素（streptozotocin，STZ）诱导糖尿病大鼠认知障碍模型，采用基因芯片技术分析对照组和STZ治疗组大鼠海马组织中lncRNA和mRNA的差异。结果STZ处理后，糖尿病大鼠海马lncRNA Vof-16和Gnb 3 mRNA表达显著上调，芯片分析显示Vof-16和miR-205具有相同的miRNA应答元件（MRE）。此外，Vof-16在原代海马神经元中的过表达抑制了miR-205的表达，反之亦然。双荧光素酶实验证实Vof-16与miR-205结合，Vof-16通过海绵状作用促进原代海马神经元增殖。硅分析预测miR-205可以与Gnb 3结合，双荧光素酶分析证实了这一点，miR-205的过表达可以抑制Gnb 3的蛋白水平，而与Vof-16共表达可以挽救Gnb 3的蛋白水平。总之，lncRNA Vof-16通过竞争性结合miR-205调节Gnb 3表达。结论这些结果为STZ诱导的糖尿病的发病机制提供了新的调控轴。
Background Diabetes is a chronic metabolic disease and an independent risk factor for cognitive damage. Non-protein coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are involved in various pathophysiological conditions. Methods In this study, cognitive impairment was induced in diabetics rats by streptozotocin (STZ) injection, and the differential lncRNAs and mRNAs in rat hippocampal tissue between control and STZ-treated groups were analyzed with microarray. Results In the hippocampus of STZ-treated diabetic rats, lncRNA Vof-16, and Gnb3 mRNA were significantly upregulated and silicon analysis showed that Vof-16 and miR-205 share the same miRNA response element (MRE). In addition, the overexpression of Vof-16 in primary hippocampal neurons inhibited the expression of miR-205, and vice versa. Dual luciferase assay verified the binding between Vof-16 and miR-205, and Vof-16 was seen to promote the proliferation of primary hippocampal neurons via sponging miR-205. Silicon analysis predicted that miR-205 could bind with Gnb3, which was verified with dual luciferase assay, and the overexpression of miR-205 could inhibit the protein level of Gnb3, which could be rescued by co-expression with Vof-16. In conclusion, lncRNA Vof-16 regulated Gnb3 expression by competitively binding to miR-205. Conclusions These results provided a novel regulation axis for the pathogenesis of STZ-induced diabetes.
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2.9
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