The relationship between SNPS in the genes of TLR signal transduction pathway downstream elements and rheumatoid arthritis susceptibility

Liu, X.; Xu, Jun; Hu, Cong; Pan, Zhencun; Zhang, Y. C.

doi:10.3103/s0095452714030074

Cited by 4 publications

(2 citation statements)

References 36 publications

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“…Biglycan is overexpressed in gastric cancer and can increase the VEGF level in endothelial cells via activation of the TLR signaling pathway, consequently inducing tumor angiogenesis (L. Hu et al, ). More important, the TLR signaling pathway has been highlighted due to its role in the induction and regulation of the innate immune system or adaptive immune responses (Liu, Xu, Hu, Pan, & Zhang, ). Moreover, a work from Arranz et al () illustrates that TLR contributes to the expression of proinflammatory cytokines, interferons, and costimulatory molecules related to innate and adaptive immunity, and points out that the inhibition of TLR signaling pathway can treat a lot of inflammatory diseases like RA.…”

Section: Discussionmentioning

confidence: 99%

RGS1 silencing inhibits the inflammatory response and angiogenesis in rheumatoid arthritis rats through the inactivation of Toll‐like receptor signaling pathway

Tang

Zeng

et al. 2019

Journal Cellular Physiology

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Emerging evidence shows that rheumatoid arthritis (RA) progression can be induced by the activation of Toll-like receptor (TLR) signaling pathway. Regulator of G-protein signaling 1 (RGS1) is observed to be a candidate biomarker for arthritis. Accordingly, the present study aims to determine the potential effects of RGS1 mediating TLR on RA. A rat model of collagen-induced arthritis (CIA) was established to mimic the features of RA by injection of bovine type II collagen. The rats with CIA were treated with short hairpin RNA (shRNA) against RGS1 or TLR pathway activator Poly I:C to elucidate the role of RGS1 in RA progression. The inflammatory factors were measured, and the thoracic gland and spleen indexes as well as the vascular density were determined. The expression levels of RGS1, TLR3, vascular endothelial growth factor (VEGF), metalloproteinase-2 (MMP-2), MMP-9, and interleukin 1 receptorassociated kinase-4 (IRAK4) were determined. RGS1 was robustly increased in RA.The TLR signaling pathway was suppressed by RGS1 silencing. shRNA-mediated depletion of RGS1 was shown to significantly enhance thoracic gland index and inhibit the serum levels of TNF-α, IL-1β, and IL-17, spleen index, vascular density, and the expression levels of TLR3, VEGF, MMP-2, MMP-9, and IRAK4. However, when the rats with CIA were treated with Poly I:C, the trend of effects was opposite. These findings highlight that functional suppression of RGS1 inhibits the inflammatory response and angiogenesis by inactivating the TLR signaling pathway in rats with CIA,

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Section: Discussionmentioning

confidence: 99%

RGS1 silencing inhibits the inflammatory response and angiogenesis in rheumatoid arthritis rats through the inactivation of Toll‐like receptor signaling pathway

Tang

Zeng

et al. 2019

Journal Cellular Physiology

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“…Members of the TLR family recognize and bind to their corresponding ligand to activate signal transduction pathways and thus produce different biological functions in response to various stimuli[13]. TLR4 is the first reported TLR by which the mediated signal pathway can non-specifically bind in pathogen-associated molecular patterns[14].…”

Section: Introductionmentioning

confidence: 99%

Effects of ω-3 fatty acids on toll-like receptor 4 and nuclear factor-κB p56 in lungs of rats with severe acute pancreatitis

Wang

Guo

et al. 2016

WJG

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AIMTo determine the effects of ω-3 fatty acids (ω-3FA) on the toll-like receptor 4 (TLR4)/nuclear factor κB p56 (NF-κBp56) signal pathway in the lungs of rats with severe acute pancreatitis (SAP).METHODSA total of 56 Sprague-Dawley rats were randomly divided into 4 groups: control group, SAP-saline group, SAP-soybean oil group and SAP-ω-3FA group. SAP was induced by the retrograde infusion of sodium taurocholate into the pancreatic duct. The expression of TLR4 and NF-κBp56 in the lungs was evaluated by immunohistochemistry and Western blot analysis. The levels of inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha in the lungs were measured by enzyme-linked immunosorbent assay.RESULTSThe expression of TLR4 and NF-κBp56 in lungs and of inflammatory cytokines in serum significantly increased in the SAP group compared with the control group (P < 0.05), but was significantly decreased in the ω-3FA group compared with the soybean oil group at 12 and 24 h (P < 0.05).CONCLUSIONDuring the initial stage of SAP, ω-3FA can efficiently lower the inflammatory response and reduce lung injury by triggering the TLR4/NF-κBp56 signal pathway.

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Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis

Aluko

Ranganathan

2022

Methods in Molecular Biology

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The relationship between SNPS in the genes of TLR signal transduction pathway downstream elements and rheumatoid arthritis susceptibility

Cited by 4 publications

References 36 publications

RGS1 silencing inhibits the inflammatory response and angiogenesis in rheumatoid arthritis rats through the inactivation of Toll‐like receptor signaling pathway

RGS1 silencing inhibits the inflammatory response and angiogenesis in rheumatoid arthritis rats through the inactivation of Toll‐like receptor signaling pathway

Effects of ω-3 fatty acids on toll-like receptor 4 and nuclear factor-κB p56 in lungs of rats with severe acute pancreatitis

Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis

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