Circ_0068087 Promotes High Glucose-Induced Human Renal Tubular Cell Injury through Regulating miR-106a-5p/ROCK2 Pathway

Experimental Nephrology and Genetics: Research Article

Feng F.a· Yang J.b· Wang G.b· Huang P.b· Li Y.a· Zhou B.b

Author affiliations

aSchool of Pharmacy, Shaoyang University, Shaoyang, China
bDepartment of Endocrinology, The Central Hospital of Shaoyang, Shaoyang, China

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Article / Publication Details

First-Page Preview

Abstract of Experimental Nephrology and Genetics: Research Article

Received: December 08, 2021
Accepted: May 27, 2022
Published online: July 22, 2022

Number of Print Pages: 11
Number of Figures: 8
Number of Tables: 2

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

For additional information: https://www.karger.com/NEF

Abstract

Background: Many studies have confirmed that circular RNA (circRNA) is an important target for regulating human disease progression. This study aimed to explore the role of circ_0068087 in diabetic nephropathy (DN) progression. Methods: High glucose (HG)-induced renal tubular cells (HK2) were used to mimic DN cell models in vitro. The expression levels of circ_0068087, microRNA (miR)-106a-5p, and Rho-associated coiled-coil-containing kinase 2 (ROCK2) were detected by quantitative real-time PCR. Cell proliferation and apoptosis were examined by cell counting kit-8 assay, 5-ethynyl-2′-deoxyuridine assay, colony formation assay, and flow cytometry. The protein levels were examined by Western blot analysis. Cell oxidative stress was assessed by measuring MDA level and SOD activity, and cell inflammation was evaluated by detecting the concentrations of inflammatory factors. RNA interaction was verified by dual-luciferase reporter assay and RNA pull-down assay. Results: The present study showed that circ_0068087 was highly expressed in the serum of DN patients and HG-induced HK2 cells. Interference of circ_0068087 alleviated HG-induced apoptosis, oxidative stress, inflammation, and fibrosis in HK2 cells, while accelerated cell proliferation. miR-106a-5p could be sponged by circ_0068087, and its inhibitor eliminated the regulation of circ_0068087 knockdown on HG-induced HK2 cell injury. ROCK2 was a target of miR-106a-5p, and its expression was suppressed by circ_0068087 knockdown. miR-106a-5p overexpression suppressed HG-induced HK2 cell injury, and this effect was reversed by ROCK2 upregulation. Conclusion: Our data indicated that circ_0068087 downregulation mitigated HG-induced HK2 cell injury through the miR-106a-5p/ROCK2 axis, providing a potential circRNA-targeted therapy for DN.

© 2022 S. Karger AG, Basel

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First-Page Preview

Abstract of Experimental Nephrology and Genetics: Research Article

Received: December 08, 2021
Accepted: May 27, 2022
Published online: July 22, 2022

Number of Print Pages: 11
Number of Figures: 8
Number of Tables: 2

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

For additional information: https://www.karger.com/NEF

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