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环状 RNA_000166/miR-296 通过调控肾近端小管上皮细胞中 SGLT2 信号通路加重糖尿病肾病纤维化。

circ_000166/miR-296 Aggravates the Process of Diabetic Renal Fibrosis by Regulating the SGLT2 Signaling Pathway in Renal Tubular Epithelial Cells.

机构信息

Department of Nephrology, Ningbo Medical Center Lihuili Hospital, Ningbo, Zhejiang 315000, China.

出版信息

Dis Markers. 2022 May 16;2022:6103086. doi: 10.1155/2022/6103086. eCollection 2022.

DOI:10.1155/2022/6103086
PMID:35615399
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9126678/
Abstract

Diabetic renal fibrosis is a common cause of end-stage renal disease, and the circRNA-miRNA-mRNA network may play an important role in the progression of diabetic nephropathy- (DN-) induced renal fibrosis. In this study, the role of circ_000166/miR-296/SGLT2 in the process of DN-related renal fibrosis was studied by constructing an animal model of DN renal fibrosis via lentiviral transfection, plasmid transfection, and dual-luciferase reporting techniques. Compared with that of normal controls, the expression of circ_000166 in the kidney tissues of DN renal fibrosis mice substantially increased. Silencing circ_000166 could minimize kidney damage and decrease urine protein levels, thereby inhibiting the progression of renal fibrosis. Moreover, circ_000166 could act as the ceRNA of miR-296 and competitively bind to miR-296, leading to an increase in the expression of the SGLT2 gene regulated by miR-296. Through mutual verification via in vivo and in vitro experiments, miR-296 was overexpressed and SGLT2 was silenced. Results showed that DN renal fibrosis and cell apoptosis were considerably reduced. We postulate that circ_000166/miR-296/SGLT2 may become a new target in the progression of DN renal fibrosis, and the regulation of this pathway may be a promising strategy for clinical treatment of DN renal fibrosis.

摘要

糖尿病肾病纤维化是终末期肾病的常见原因，而 circRNA-miRNA-mRNA 网络可能在糖尿病肾病（DN）诱导的肾纤维化进展中发挥重要作用。在这项研究中，通过慢病毒转染、质粒转染和双荧光素酶报告技术构建了 DN 肾纤维化动物模型，研究了 circ_000166/miR-296/SGLT2 在 DN 相关肾纤维化过程中的作用。与正常对照组相比，DN 肾纤维化小鼠肾组织中 circ_000166 的表达显著增加。沉默 circ_000166 可以最小化肾脏损伤并降低尿蛋白水平，从而抑制肾纤维化的进展。此外，circ_000166 可以作为 miR-296 的 ceRNA，并与 miR-296 竞争结合，导致受 miR-296 调节的 SGLT2 基因表达增加。通过体内和体外实验的相互验证，过表达 miR-296 并沉默 SGLT2。结果表明，DN 肾纤维化和细胞凋亡明显减少。我们推测 circ_000166/miR-296/SGLT2 可能成为 DN 肾纤维化进展的新靶点，该通路的调节可能是治疗 DN 肾纤维化的有前途的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/da53f2acb883/DM2022-6103086.006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/ae834f8846df/DM2022-6103086.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/da53f2acb883/DM2022-6103086.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/350676fec01a/DM2022-6103086.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/d10286fd21c9/DM2022-6103086.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/d01d8de7d1ec/DM2022-6103086.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/242e24bfbc63/DM2022-6103086.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/ae834f8846df/DM2022-6103086.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5e1/9126678/da53f2acb883/DM2022-6103086.006.jpg

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