C-Reactive Protein Promotes Inflammation through TLR-4/NF-κB/TGF-β Pathway in HL-1 Cells

Bioscience Reports
Weiping SunXingpeng Liu

Abstract

Atrial fibrillation (AF) is the most common type of heart arrhythmia. Currently the pathogenesis of AF is not fully understood yet. A growing body of evidence highlighted the strong association between inflammation and the pathogenesis of AF. C-reactive protein (CRP) is an inflammation marker with increased expression in AF. Therefore, the aim of this study was to determine if CRP promotes inflammation, which may sequentially mediate the onset of AF and the concurrent atrial fibrosis, through TLR4/NF-κB/TGF-β pathway. HL-1 cells were treated with either 25 μg/ml or 50 μg/ml recombinant human CRP. TGF-β1 and NF-κB inhibitors were given either solely or together to the 50 μg/ml-CRP treated cells. Cell proliferation, apoptosis, the expression of apoptotic factors and TLR4, IL-6, TGF-β1, Smad2, and the phosphorylation of Smad2 were determined. Data showed that CRP induced dose-dependent inhibition on cell proliferation and promoted cell apoptosis, which was induced through both intrinsic and extrinsic pathways. Such effects were reversed by inhibiting TGF-β1 and/or NF-κB. Inhibition of TGF-β1 and/or NF-κB also reduced the expression of TLR4 and IL-6. Inhibition of NF-κB alone weakened the expression of TGF-β1 and phosphorylation of...Continue Reading

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Citations

Oct 31, 2020·Clinical and Experimental Dental Research·Harriet LarvinJianhua Wu
Mar 9, 2021·Frontiers in Immunology·Ahmed SheriffBirgit Vogt
Oct 2, 2021·Acta Biochimica Et Biophysica Sinica·Hechuan WangHua Xiao

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Methods Mentioned

BETA
electrophoresis
nuclear translocation

Software Mentioned

GraphPad Prism

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