CARD6 protects against collagen-induced rheumatoid arthritis in mice through attenuating the inflammatory response and joint destruction via suppression of TNFR1/TRAF2 signaling

Zhao, Min; He, Haiyang; Yin, Jianbao

doi:10.1016/j.bbrc.2020.04.006

Cited by 6 publications

(3 citation statements)

References 34 publications

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“…IL-6 and the cognate IL-6R produced after collagen type II immunization contribute to the pathogenesis of RA [ 29 ]. In addition, the TNF/TNFR pathway plays a prominent role in the pathogenesis of chronic inflammatory diseases and autoimmune disorders [ 30 ]. Therefore, we evaluated whether IL-6R and TNFR1 decreased in CIA+PEMF mice.…”

Section: Resultsmentioning

confidence: 99%

Pulsed Electromagnetic Field (PEMF) Treatment Ameliorates Murine Model of Collagen-Induced Arthritis

Hong

Lee

Hwang

et al. 2023

IJMS

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Rheumatoid arthritis (RA) is an autoimmune disease of the joint synovial membranes. RA is difficult to prevent or treat; however, blocking proinflammatory cytokines is a general therapeutic strategy. Pulsed electromagnetic field (PEMF) is reported to alleviate RA’s inflammatory response and is being studied as a non-invasive physical therapy. In this current study, PEMF decreased paw inflammation in a collagen-induced arthritis (CIA) murine model. PEMF treatment at 10 Hz was more effective in ameliorating arthritis than at 75 Hz. In the PEMF-treated CIA group, the gross inflammation score and cartilage destruction were lower than in the untreated CIA group. The CIA group treated with PEMF also showed lower serum levels of IL-1β but not IL-6, IL-17, or TNF-α. Serum levels of total anti-type II collagen IgG and IgG subclasses (IgG1, IgG2a, and IgG2b) remained unchanged. In contrast, tissue protein levels of IL-1β, IL-6, TNF-α, receptor activator of nuclear factor kappa-Β (RANK), RANK ligand (RANKL), IL-6 receptor (IL-6R), and TNF-α receptor1 (TNFR1) were all lower in the ankle joints of the PEMF-treated CIA group compared with the CIA group. The results of this study suggest that PEMF treatment can preserve joint morphology cartilage and delay the occurrence of CIA. PEMF has potential as an effective adjuvant therapy that can suppress the progression of RA.

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Section: Resultsmentioning

confidence: 99%

Pulsed Electromagnetic Field (PEMF) Treatment Ameliorates Murine Model of Collagen-Induced Arthritis

Hong

Lee

Hwang

et al. 2023

IJMS

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“…The encoded protein is microtubule-associated and positively modulates signal transduction, which leads to activation of NF-κB [61]. Recent work demonstrated that the over-expression of Card6 suppressed rheumatoid inflammation and NF-κB activity [62]. Card6 was an important protective factor in spinal cord injury progression, limiting the inflammatory response in mice by suppressing NF-κB-mediated enhancement of pro-inflammatory cytokines [63].…”

Section: Common Pathwaymentioning

confidence: 99%

Molecular Mechanisms for Changing Brain Connectivity in Mice and Humans

Voelker,

Weible,

Niell

et al. 2023

IJMS

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The goal of this study was to examine commonalities in the molecular basis of learning in mice and humans. In previous work we have demonstrated that the anterior cingulate cortex (ACC) and hippocampus (HC) are involved in learning a two-choice visuospatial discrimination task. Here, we began by looking for candidate genes upregulated in mouse ACC and HC with learning. We then determined which of these were also upregulated in mouse blood. Finally, we used RT-PCR to compare candidate gene expression in mouse blood with that from humans following one of two forms of learning: a working memory task (network training) or meditation (a generalized training shown to change many networks). Two genes were upregulated in mice following learning: caspase recruitment domain-containing protein 6 (Card6) and inosine monophosphate dehydrogenase 2 (Impdh2). The Impdh2 gene product catalyzes the first committed step of guanine nucleotide synthesis and is tightly linked to cell proliferation. The Card6 gene product positively modulates signal transduction. In humans, Card6 was significantly upregulated, and Impdh2 trended toward upregulation with training. These genes have been shown to regulate pathways that influence nuclear factor kappa B (NF-κB), a factor previously found to be related to enhanced synaptic function and learning.

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“…In contrast, overexpression of CARD6 results in decreased expression of pro-inflammatory factors and chemokines in addition to inhibition of TNFR1/tumor necrosis factor receptor-associated factor-2 (TRAF2)/NF-kB signaling pathway, which alleviates not only the TNF-a induced inflammation and apoptosis of macrophages but also the level of bone destruction in CIA mice. Furthermore, it inhibits the activation of cleaved caspase-3, indicating that CARD6 plays an anti-inflammatory and anti-apoptotic role in RA (85). The high expression of SH3s may be involved in the protection and survival of synovial cells as well as stimulation of cell proliferation (86).…”

Section: Decreased Apoptosis Of Pro-inflammatory Cell Subtypes Exacerbates the Ra Associated Inflammation And Bone Destructionmentioning

confidence: 99%

Apoptosis, Autophagy, NETosis, Necroptosis, and Pyroptosis Mediated Programmed Cell Death as Targets for Innovative Therapy in Rheumatoid Arthritis

et al. 2021

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Rheumatoid arthritis (RA) is a chronic inflammatory joint disease that can lead to clinical manifestations of systemic diseases. Its leading features include chronic synovial inflammation and degeneration of the bones and joints. In the past decades, multiple susceptibilities for rheumatoid arthritis have been identified along with the development of a remarkable variety of drugs for its treatment; which include analgesics, glucocorticoids, nonsteroidal anti-inflammatory medications (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic response modifiers (bDMARDs). Despite the existence of many clinical treatment options, the prognosis of some patients remains poor due to complex mechanism of the disease. Programmed cell death (PCD) has been extensively studied and ascertained to be one of the essential pathological mechanisms of RA. Its dysregulation in various associated cell types contributes to the development of RA. In this review, we summarize the role of apoptosis, cell death-associated neutrophil extracellular trap formation, necroptosis, pyroptosis, and autophagy in the pathophysiology of RA to provide a theoretical reference and insightful direction to the discovery and development of novel therapeutic targets for RA.

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CARD6 protects against collagen-induced rheumatoid arthritis in mice through attenuating the inflammatory response and joint destruction via suppression of TNFR1/TRAF2 signaling

Cited by 6 publications

References 34 publications

Pulsed Electromagnetic Field (PEMF) Treatment Ameliorates Murine Model of Collagen-Induced Arthritis

Pulsed Electromagnetic Field (PEMF) Treatment Ameliorates Murine Model of Collagen-Induced Arthritis

Molecular Mechanisms for Changing Brain Connectivity in Mice and Humans

Apoptosis, Autophagy, NETosis, Necroptosis, and Pyroptosis Mediated Programmed Cell Death as Targets for Innovative Therapy in Rheumatoid Arthritis

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