MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB Pathway

This study was designed to explore the specific mechanism of miR-429 in neuroinflammation of TS, to provide a theoretical basis for the etiology of TS and new targets for future treatment. Male SD rats were randomly divided into the normal control (CON) group and the Tourette syndrome (TS) group. Th...

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Main Authors: Zhongling Ke, Yanhui Chen, Xiaoxia Lin, Jilong Jiang
Format: Article
Language:English
Published: Wiley 2025-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/mi/7165782
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author Zhongling Ke
Yanhui Chen
Xiaoxia Lin
Jilong Jiang
author_facet Zhongling Ke
Yanhui Chen
Xiaoxia Lin
Jilong Jiang
author_sort Zhongling Ke
collection DOAJ
description This study was designed to explore the specific mechanism of miR-429 in neuroinflammation of TS, to provide a theoretical basis for the etiology of TS and new targets for future treatment. Male SD rats were randomly divided into the normal control (CON) group and the Tourette syndrome (TS) group. The activation of microglia in the striatum was detected by immunohistochemistry and the concentration of interleukin (IL)-6 in the brain was measured by ELISA. The expression of miR-429 in brains was detected by quantitative real-time PCR (qPCR). Human microglia clone 3 (HMC3) cells were transfected, respectively, with double-stranded inactive miRNA; miR-429 mimics; miR-429 inhibitors. The levels of miR-429 and IKKβ mRNA were detected by qPCR. The expression levels of IKKβ, NF-κBp65 b, and IL-6 proteins were detected by western blot. MiR-429 and IKKβ targeted binding was verified by a double luciferase experiment. IL-6 in the brain of the TS rat group was higher than in the CON group. Furthermore, the relative expression of miR-429 in the TS group was several hundreds of times higher than in the CON group. The levels of IKKβ, NF-κBp65, and IL-6 protein in lipopolysaccharide (LPS)-induced microglia were lower in the miR-429 mimics group, but higher in the miR-429 inhibitor group, compared to those of the MiRNA negative control (miR-NC) group (p<0.05). The miR-429 targeted IKKβ binding to regulate the NF-κB pathway and inhibit the release of pro-inflammatory factors, thus, controlling neuroinflammation in microglia, which may be the mechanism of action of miR-429 in TS.
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spelling doaj-art-8b9e098ba68a4ccab493e8a8614780102025-08-20T03:58:35ZengWileyMediators of Inflammation1466-18612025-01-01202510.1155/mi/7165782MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB PathwayZhongling Ke0Yanhui Chen1Xiaoxia Lin2Jilong Jiang3Fujian Medical University Union HospitalFujian Medical University Union HospitalFujian Medical University Union HospitalFujian Medical University Union HospitalThis study was designed to explore the specific mechanism of miR-429 in neuroinflammation of TS, to provide a theoretical basis for the etiology of TS and new targets for future treatment. Male SD rats were randomly divided into the normal control (CON) group and the Tourette syndrome (TS) group. The activation of microglia in the striatum was detected by immunohistochemistry and the concentration of interleukin (IL)-6 in the brain was measured by ELISA. The expression of miR-429 in brains was detected by quantitative real-time PCR (qPCR). Human microglia clone 3 (HMC3) cells were transfected, respectively, with double-stranded inactive miRNA; miR-429 mimics; miR-429 inhibitors. The levels of miR-429 and IKKβ mRNA were detected by qPCR. The expression levels of IKKβ, NF-κBp65 b, and IL-6 proteins were detected by western blot. MiR-429 and IKKβ targeted binding was verified by a double luciferase experiment. IL-6 in the brain of the TS rat group was higher than in the CON group. Furthermore, the relative expression of miR-429 in the TS group was several hundreds of times higher than in the CON group. The levels of IKKβ, NF-κBp65, and IL-6 protein in lipopolysaccharide (LPS)-induced microglia were lower in the miR-429 mimics group, but higher in the miR-429 inhibitor group, compared to those of the MiRNA negative control (miR-NC) group (p<0.05). The miR-429 targeted IKKβ binding to regulate the NF-κB pathway and inhibit the release of pro-inflammatory factors, thus, controlling neuroinflammation in microglia, which may be the mechanism of action of miR-429 in TS.http://dx.doi.org/10.1155/mi/7165782
spellingShingle Zhongling Ke
Yanhui Chen
Xiaoxia Lin
Jilong Jiang
MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB Pathway
Mediators of Inflammation
title MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB Pathway
title_full MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB Pathway
title_fullStr MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB Pathway
title_full_unstemmed MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB Pathway
title_short MicroRNA-429 Inhibits Microglial Inflammation by Targeting IKKβ Through the NF-κB Pathway
title_sort microrna 429 inhibits microglial inflammation by targeting ikkβ through the nf κb pathway
url http://dx.doi.org/10.1155/mi/7165782
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AT yanhuichen microrna429inhibitsmicroglialinflammationbytargetingikkbthroughthenfkbpathway
AT xiaoxialin microrna429inhibitsmicroglialinflammationbytargetingikkbthroughthenfkbpathway
AT jilongjiang microrna429inhibitsmicroglialinflammationbytargetingikkbthroughthenfkbpathway