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Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis

Circular RNAs (circRNAs) are involved in the progression of various diseases, including lupus nephritis. Hsa_circ_0010957 is reported to be dysregulated in lupus nephritis, but the exact function of this circRNA is unknown. This research aims to study the function and mechanism of circRNA hsa_circ_0...

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Autores principales: Pan, Jiaojiao, Wang, Xiujie, Cang, Xiaofeng, Jiang, Yizhen, Tang, Ruoyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8574102/
https://www.ncbi.nlm.nih.gov/pubmed/34764803
http://dx.doi.org/10.5114/ceji.2021.108772
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author Pan, Jiaojiao
Wang, Xiujie
Cang, Xiaofeng
Jiang, Yizhen
Tang, Ruoyu
author_facet Pan, Jiaojiao
Wang, Xiujie
Cang, Xiaofeng
Jiang, Yizhen
Tang, Ruoyu
author_sort Pan, Jiaojiao
collection PubMed
description Circular RNAs (circRNAs) are involved in the progression of various diseases, including lupus nephritis. Hsa_circ_0010957 is reported to be dysregulated in lupus nephritis, but the exact function of this circRNA is unknown. This research aims to study the function and mechanism of circRNA hsa_circ_0010957 in a lipopolysaccharide (LPS)-induced cellular model of lupus nephritis. Human renal proximal tubular cell line HK2 cells were challenged by LPS. Hsa_circ_0010957, microRNA-1224-5p (miR-1224-5p), and interleukin-1 receptor-associated kinase 1 (IRAK1) abundances were examined by quantitative reverse transcription polymerase chain reaction or western blot. LPS-induced damage was evaluated via cell viability, apoptosis, inflammatory response and oxidative injury. The target interaction was analyzed by dual-luciferase reporter analysis and RNA immunoprecipitation. Hsa_circ_0010957 abundance was enhanced in LPS-challenged HK2 cells. Hsa_circ_0010957 knockdown alleviated LPS-induced apoptosis, the inflammatory response and oxidative injury in HK2 cells. MiR-1224-5p was targeted by hsa_circ_0010957, and miR-1224-5p knockdown reversed the influence of hsa_circ_0010957 silence on LPS-induced injury. IRAK1 was targeted via miR-1224-5p, and hsa_circ_0010957 could regulate IRAK1 by miR-1224-5p. MiR-1224-5p overexpression could mitigate LPS-induced apoptosis, the inflammatory response and oxidative injury, and this effect was abolished by IRAK1. Hsa_circ_0010957 silence weakened LPS-induced HK2 cell apoptosis, the inflammatory response and oxidative injury via regulating the miR-1224-5p/IRAK1 axis.
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spelling pubmed-85741022021-11-10 Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis Pan, Jiaojiao Wang, Xiujie Cang, Xiaofeng Jiang, Yizhen Tang, Ruoyu Cent Eur J Immunol Experimental Immunology Circular RNAs (circRNAs) are involved in the progression of various diseases, including lupus nephritis. Hsa_circ_0010957 is reported to be dysregulated in lupus nephritis, but the exact function of this circRNA is unknown. This research aims to study the function and mechanism of circRNA hsa_circ_0010957 in a lipopolysaccharide (LPS)-induced cellular model of lupus nephritis. Human renal proximal tubular cell line HK2 cells were challenged by LPS. Hsa_circ_0010957, microRNA-1224-5p (miR-1224-5p), and interleukin-1 receptor-associated kinase 1 (IRAK1) abundances were examined by quantitative reverse transcription polymerase chain reaction or western blot. LPS-induced damage was evaluated via cell viability, apoptosis, inflammatory response and oxidative injury. The target interaction was analyzed by dual-luciferase reporter analysis and RNA immunoprecipitation. Hsa_circ_0010957 abundance was enhanced in LPS-challenged HK2 cells. Hsa_circ_0010957 knockdown alleviated LPS-induced apoptosis, the inflammatory response and oxidative injury in HK2 cells. MiR-1224-5p was targeted by hsa_circ_0010957, and miR-1224-5p knockdown reversed the influence of hsa_circ_0010957 silence on LPS-induced injury. IRAK1 was targeted via miR-1224-5p, and hsa_circ_0010957 could regulate IRAK1 by miR-1224-5p. MiR-1224-5p overexpression could mitigate LPS-induced apoptosis, the inflammatory response and oxidative injury, and this effect was abolished by IRAK1. Hsa_circ_0010957 silence weakened LPS-induced HK2 cell apoptosis, the inflammatory response and oxidative injury via regulating the miR-1224-5p/IRAK1 axis. Termedia Publishing House 2021-09-28 2021 /pmc/articles/PMC8574102/ /pubmed/34764803 http://dx.doi.org/10.5114/ceji.2021.108772 Text en Copyright © 2021 Termedia https://creativecommons.org/licenses/by-nc-sa/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0). License (http://creativecommons.org/licenses/by-nc-sa/4.0/ (https://creativecommons.org/licenses/by-nc-sa/4.0/) )
spellingShingle Experimental Immunology
Pan, Jiaojiao
Wang, Xiujie
Cang, Xiaofeng
Jiang, Yizhen
Tang, Ruoyu
Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis
title Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis
title_full Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis
title_fullStr Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis
title_full_unstemmed Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis
title_short Hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced HK2 cell injury by regulating the miR-1224-5p/IRAK1 axis
title_sort hsa_circ_0010957 knockdown attenuates lipopolysaccharide-induced hk2 cell injury by regulating the mir-1224-5p/irak1 axis
topic Experimental Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8574102/
https://www.ncbi.nlm.nih.gov/pubmed/34764803
http://dx.doi.org/10.5114/ceji.2021.108772
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