LncRNA LINC01197 inhibited the formation of calcium oxalate-induced kidney stones by regulating miR-516b-5p/SIRT3/FOXO1 signaling pathway
LncRNA LINC01197 inhibited the formation of calcium oxalate-induced kidney stones by regulating miR-516b-5p/SIRT3/FOXO1 signaling pathway
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DOI：
10.1007/s00441-022-03734-6
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发表时间：
2023-01
影响因子：
3.6
通讯作者：
J. Xi;Yang Chen;J. Jing;Wei Qi;Yanbin Zhang
中科院分区：
文献类型：
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作者：
J. Xi;Yang Chen;J. Jing;Wei Qi;Yanbin Zhang
长链非编码 RNA (lncRNA) 在调节草酸钙 (CaOx) 晶体诱导的肾结石形成和沉积中发挥着关键作用。本研究的目的是研究lncRNA LINC01197对CaOx诱导的肾结石形成的影响及其潜在机制。通过分析Ca2+浓度来评估HK-2细胞中的晶体细胞粘附。通过流式细胞术检测细胞凋亡。采用RT-qPCR和western blot检测mRNA和蛋白表达。肾结石患者的 LINC01197 和 SIRT3 表达下调，而 miR-516b-5p 表达上调。 LINC01197敲除促进CaOx诱导的细胞粘附和细胞凋亡，增加Bax，减少Bcl-2表达。荧光素酶报告基因检测显示，LINC01197 与 miR-516b-5p 竞争结合可促进 SIRT3 表达。此外，SIRT3/FOXO1过表达会促进LINC01197的表达，并且可以通过FOXO1敲低来逆转。总之，本研究表明，lncRNA LINC01197 通过调节 miR-516b-5p/SIRT3/FOXO1 信号通路抑制 CaOx 诱导的肾结石形成。
Long non-coding RNA (lncRNA) plays a key role in the regulation of calcium oxalate (CaOx) crystals-induced kidney stone formation and deposition. The purpose of this study is to study the effect of lncRNA LINC01197 on CaOx-induced kidney stone formation and the underlying mechanism. Crystal cell adhesion in HK-2 cells was evaluated by analyzing Ca2+ concentration. Apoptosis was detected by flow cytometry. The RT-qPCR and western blot were used to detect the mRNA and protein expression. Patients with kidneys stones showed down-regulated LINC01197 and SIRT3 expression, and up-regulated miR-516b-5p expression. LINC01197 knockdown promoted CaOx-induced cell adherence and cell apoptosis, increased Bax, decreased Bcl-2 expression. Luciferase reporter assay showed that SIRT3 expression was promoted by LINC01197 competing binds to miR-516b-5p. In addition, LINC01197 expression was promoted by SIRT3/FOXO1 overexpression, and could be reversed by FOXO1 knockdown. In conclusion, the present study revealed that lncRNA LINC01197 inhibited CaOx-induced kidney stones formation by regulating the miR-516b-5p/SIRT3/FOXO1 signaling pathway.