Research progress of NF-κB signaling pathway and thrombosis

Wang, Zilong; Fang, Chucun; Yao, Mengting; Wu, Dongwen; Chen, Maga; Guo, Tianting; Mo, Jianwen

doi:10.3389/fimmu.2023.1257988

Cited by 15 publications

(4 citation statements)

References 133 publications

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“…Furthermore, our data showed than upon NKS3 stimulation, GPR120 forms a complex with β-arrestin and TAB1. The formation of this complex results in the diminution of TAB1/TAK1 interaction and thus a decrease, by NKS3, in TAK1 phosphorylation in cells treated with LPS, leading to the inhibition of the NF-kB, a key regulator of inflammation and inflammatory diseases [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

A novel fatty acid analogue triggers CD36–GPR120 interaction and exerts anti-inflammatory action in endotoxemia

Boutanquoi,

Khan,

Cabeza

et al. 2024

Cell. Mol. Life Sci.

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Inflammation is a mediator of a number of chronic pathologies. We synthesized the diethyl (9Z,12Z)-octadeca-9,12-dien-1-ylphosphonate, called NKS3, which decreased lipopolysaccharide (LPS)-induced mRNA upregulation of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) not only in primary intraperitoneal and lung alveolar macrophages, but also in freshly isolated mice lung slices. The in-silico studies suggested that NKS3, being CD36 agonist, will bind to GPR120. Co-immunoprecipitation and proximity ligation assays demonstrated that NKS3 induced protein–protein interaction of CD36 with GPR120in RAW 264.7 macrophage cell line. Furthermore, NKS3, via GPR120, decreased LPS-induced activation of TAB1/TAK1/JNK pathway and the LPS-induced mRNA expression of inflammatory markers in RAW 264.7 cells. In the acute lung injury model, NKS3 decreased lung fibrosis and inflammatory cytokines (IL-1β, IL-6 and TNF-α) and nitric oxide (NO) production in broncho-alveolar lavage fluid. NKS3 exerted a protective effect on LPS-induced remodeling of kidney and liver, and reduced circulating IL-1β, IL-6 and TNF-α concentrations. In a septic shock model, NKS3 gavage decreased significantly the LPS-induced mortality in mice. In the last, NKS3 decreased neuroinflammation in diet-induced obese mice. Altogether, these results suggest that NKS3 is a novel anti-inflammatory agent that could be used, in the future, for the treatment of inflammation-associated pathologies.

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Section: Discussionmentioning

confidence: 99%

A novel fatty acid analogue triggers CD36–GPR120 interaction and exerts anti-inflammatory action in endotoxemia

Boutanquoi,

Khan,

Cabeza

et al. 2024

Cell. Mol. Life Sci.

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“…The activation of NF‐κB signaling pathway plays crucial roles in various biological processes, including immune response, inflammation, and apoptosis. 87 , 88 Radiation exposure triggers inflammatory response in radiation‐induced brain injury, releasing cytokines, such as TNF‐α, IL‐1β, and IL‐6. 15 , 19 Following irradiation, the NF‐κB p65 subunit underwent nuclear translocation, and there was a significant upregulation of essential modulator (NEMO) and a significant decrease in inhibitor of NF‐κB regulation‐α.…”

Section: Signal Pathways Of Microglia In Radiation‐induced Brain Injurymentioning

confidence: 99%

Microglia in radiation‐induced brain injury: Cellular and molecular mechanisms and therapeutic potential

Wang,

Tian,

Liu

et al. 2024

CNS Neurosci Ther

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BackgroundRadiation‐induced brain injury is a neurological condition resulting from radiotherapy for malignant tumors, with its underlying pathogenesis still not fully understood. Current hypotheses suggest that immune cells, particularly the excessive activation of microglia in the central nervous system and the migration of peripheral immune cells into the brain, play a critical role in initiating and progressing the injury. This review aimed to summarize the latest advances in the cellular and molecular mechanisms and the therapeutic potential of microglia in radiation‐induced brain injury.MethodsThis article critically examines recent developments in understanding the role of microglia activation in radiation‐induced brain injury. It elucidates associated mechanisms and explores novel research pathways and therapeutic options for managing this condition.ResultsPost‐irradiation, activated microglia release numerous inflammatory factors, exacerbating neuroinflammation and facilitating the onset and progression of radiation‐induced damage. Therefore, controlling microglial activation and suppressing the secretion of related inflammatory factors is crucial for preventing radiation‐induced brain injury. While microglial activation is a primary factor in neuroinflammation, the precise mechanisms by which radiation prompts this activation remain elusive. Multiple signaling pathways likely contribute to microglial activation and the progression of radiation‐induced brain injury.ConclusionsThe intricate microenvironment and molecular mechanisms associated with radiation‐induced brain injury underscore the crucial roles of immune cells in its onset and progression. By investigating the interplay among microglia, neurons, astrocytes, and peripheral immune cells, potential strategies emerge to mitigate microglial activation, reduce the release of inflammatory agents, and impede the entry of peripheral immune cells into the brain.

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“…NF-κB is a ubiquitous transcription factor that is particularly important for the transcriptional control of genes that participate in the response to sepsis and inflammation [ 9 ]. NF-κB is activated in different cell types by many stimulants, including viral and bacterial pathogens, and pro-inflammatory cytokines, such as interleukin (IL)-1, IL-6, IL-8, IL-12, and tumor necrosis factor (TNF)-α [ 10 ]. In this context, IL-8 plays a major role in pro-inflammatory signaling, as it is elevated in patients with Crohn’s disease or ulcerative colitis, and its levels correlate with intestinal inflammation [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

Garcia,

Makiyama,

Sampaio

et al. 2024

Metabolites

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Branched-chain amino acids (BCAA) are essential for maintaining intestinal mucosal integrity. However, only a few studies have explored the role of BCAA in the modulation of intestinal inflammation. In this study, we investigated in vitro effects of BCAA on the inflammatory response induced by lipopolysaccharide (LPS) (1 µg/mL) in Caco-2 cells. Caco-2 cells were assigned to six groups: control without BCAA (CTL0), normal BCAA (CTL; 0.8 mM leucine, 0.8 mM isoleucine, and 0.8 mM valine); leucine (LEU; 2 mM leucine), isoleucine (ISO; 2 mM isoleucine), valine (VAL; 2 mM valine), and high BCAA (LIV; 2 mM leucine, 2 mM isoleucine, and 2 mM valine). BCAA was added to the culture medium 24 h before LPS stimulation. Our results indicated that BCAA supplementation did not impair cell viability. The amino acids leucine and isoleucine attenuated the synthesis of IL-8 and JNK and NF-kB phosphorylation induced by LPS. Furthermore, neither BCAA supplementation nor LPS treatment modulated the activity of glutathione peroxidase or the intracellular reduced glutathione/oxidized glutathione ratio. Therefore, leucine and isoleucine exert anti-inflammatory effects in Caco-2 cells exposed to LPS by modulating JNK and NF-kB phosphorylation and IL-8 production. Further in vivo studies are required to validate these findings and gather valuable information for potential therapeutic or dietary interventions.

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Research progress of NF-κB signaling pathway and thrombosis

Cited by 15 publications

References 133 publications

A novel fatty acid analogue triggers CD36–GPR120 interaction and exerts anti-inflammatory action in endotoxemia

A novel fatty acid analogue triggers CD36–GPR120 interaction and exerts anti-inflammatory action in endotoxemia

Microglia in radiation‐induced brain injury: Cellular and molecular mechanisms and therapeutic potential

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

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