Tripartite Motif Containing 52 Positively Regulates NF-κB Signaling by Promoting IκBα Ubiquitination in Lipopolysaccharide-Treated Microglial Cell Activation

Zhang, Pei; Wu, Yimin; Li, Ruifeng; Lv, Huicheng; Yu, Biao

doi:10.12659/msm.925356

Cited by 4 publications

(3 citation statements)

References 31 publications

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“…9 TRIM52 activates the NF-κB signaling pathway by promoting the ubiquitination of IκBα protein, thereby promoting LPS-induced microglia activation and increasing neuroinflammation. 10 In addition, TRIM52 plays a vital role in regulating tumors as well. Overexpression of TRIM52 can promote the proliferation of colon cancer cells and inhibit apoptosis.…”

Section: Introductionmentioning

confidence: 99%

TRIM52 aggravated inflammation and pyroptosis in dextran sulfate sodium-induced inflammatory bowel disease through activation of the TLR4/NF-κBs pathway

Yao

Jia

et al. 2023

Allergol Immunopathol

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Introduction: Inflammatory bowel disease (IBD), which mainly leads to diarrhea, fatigue, stool blood, abdominal pain, and cramping, is threatening public health. Tripartite motif-containing 52 (TRIM52) has been reported to play an important role in inflammatory responses via activating the toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) pathway. However, the causes of IBD need to be elucidated, and the function of TRIM52 in IBD remains unclear. Here, we demonstrated that TRIM52 aggravated inflammation and pyroptosis in dextran sulfate sodium (DSS)-induced IBD by activating TLR4/NF-κBs pathway. Methods: The colitis model was established on mice through DSS induction. For the TRIM52 knock-down, the mice were infected with a recombinant adenoviral vector expressing sgRNAs targeting TRIM52. RT-qPCR, western blot, and immunohistochemistry were performed to verify TRIM52 expression in DSS-induced IBD. The body weight, disease activity index, colon length, and H&E staining were used to assess the IBD symptoms in mice with TRIM52 knockdown. The inflammatory responses were examined by RT-qPCR and ELISA measuring tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β). Furthermore, the pyroptosis in colon tissue was detected by western blot. Finally, the TLR4/NF-κBs pathway activity was also examined by western blot. Results: TRIM52 expression was up-regulated in DSS-induced IBD, and knockdown of TRIM52 could alleviate the symptoms of IBD. TRIM52 knockdown retarded DSS-induced inflammatory response and inhibited DSS-induced pyroptosis in colon tissue. In addition, TRIM52 played a role in activating TLR4/NF-κBs pathway. Conclusion: Knockdown of TRIM52 alleviated inflammation and pyroptosis in IBD by regulating TLR4/NF-κBs pathway. TRIM52 is expected to be a novel diagnostic indicator for IBD and a tar-get of therapeutic treatment.

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Section: Introductionmentioning

confidence: 99%

TRIM52 aggravated inflammation and pyroptosis in dextran sulfate sodium-induced inflammatory bowel disease through activation of the TLR4/NF-κBs pathway

Yao

Jia

et al. 2023

Allergol Immunopathol

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“…Studies have shown that NFKBIA can not only regulate immune inflammation and tissue damage but also be closely related to the development, differentiation, and migration of immune cells. [53][54][55] In addition, as the most important inhibitor of the nuclear factor kappa B (NF-κB) pathway, NFKBIA usually exists in the mitochondria of the cytoplasm in a relatively static state. Once stimulated by Aβ, NFKBIA will be phosphorylated and degraded, causing NF-κB activation, and leading to AD neuronal degeneration and cognitive impairment.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics-Based Approach for Exploring the Immune Cell Infiltration Patterns in Alzheimer’s Disease and Determining the Intervention Mechanism of Liuwei Dihuang Pill

et al. 2022

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Traditional Chinese medicine (TCM) compounds have recently garnered attention for the regulation of immune cell infiltration and the prevention and treatment of Alzheimer’s disease (AD). The Liuwei Dihuang Pill (LDP) has potential in this regard; however, its specific molecular mechanism currently remains unclear. Therefore, we adopted a bioinformatics approach to investigate the infiltration patterns of different types of immune cells in AD and explored the molecular mechanism of LDP intervention, with the aim of providing a new basis for improving the clinical immunotherapy of AD patients. We found that M1 macrophages showed significantly different degrees of infiltration between the hippocampal tissue samples of AD patients and healthy individuals. Four immune intersection targets of LDP in the treatment of AD were identified; they were enriched in 206 biological functions and 30 signaling pathways. Quercetin had the best docking effect with the core immune target PRKCB. Our findings suggest that infiltrated immune cells may influence the course of AD and that LDP can regulate immune cell infiltration through multi-component, multi-target, and multi-pathway approaches, providing a new research direction regarding AD immunotherapy.

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“…Conversely, in the context of Japanese Encephalitis Virus (JEV) infection of the brain, TRIM21 appears to support viral replication as it interacts with and downregulates IRF-3 in a RING-dependent manner, thereby reducing virus-restrictive type I IFN signaling ( Manocha et al, 2014 ). TRIM52 (class V), however, ubiquitinates and degrades JEV viral protein NS2A, possibly also supported by its ability to promote NF-κB signaling ( Fan et al, 2016 , 2017 ; Zhang P. et al, 2020 ). Whilst neither of these TRIMs have identifiable roles in brain development, IFN and NF-κB signaling do, as described elsewhere in this article, and their interplay with TRIM proteins remains to be fully explored in disease and developmental contexts.…”

Section: The Role Of Trims In Fighting Viruses In the Brainmentioning

confidence: 99%

It’s a TRIM-endous view from the top: the varied roles of TRIpartite Motif proteins in brain development and disease

Dudley-Fraser,

Rittinger

2023

Front. Mol. Neurosci.

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The tripartite motif (TRIM) protein family members have been implicated in a multitude of physiologies and pathologies in different tissues. With diverse functions in cellular processes including regulation of signaling pathways, protein degradation, and transcriptional control, the impact of TRIM dysregulation can be multifaceted and complex. Here, we focus on the cellular and molecular roles of TRIMs identified in the brain in the context of a selection of pathologies including cancer and neurodegeneration. By examining each disease in parallel with described roles in brain development, we aim to highlight fundamental common mechanisms employed by TRIM proteins and identify opportunities for therapeutic intervention.

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Tripartite Motif Containing 52 Positively Regulates NF-κB Signaling by Promoting IκBα Ubiquitination in Lipopolysaccharide-Treated Microglial Cell Activation

Cited by 4 publications

References 31 publications

TRIM52 aggravated inflammation and pyroptosis in dextran sulfate sodium-induced inflammatory bowel disease through activation of the TLR4/NF-κBs pathway

TRIM52 aggravated inflammation and pyroptosis in dextran sulfate sodium-induced inflammatory bowel disease through activation of the TLR4/NF-κBs pathway

Bioinformatics-Based Approach for Exploring the Immune Cell Infiltration Patterns in Alzheimer’s Disease and Determining the Intervention Mechanism of Liuwei Dihuang Pill

It’s a TRIM-endous view from the top: the varied roles of TRIpartite Motif proteins in brain development and disease

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