RGD Reference Report - C-reactive protein triggers inflammatory responses partly via TLR4/IRF3/NF-kappaB signaling pathway in rat vascular smooth muscle cells. - Rat Genome Database

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C-reactive protein triggers inflammatory responses partly via TLR4/IRF3/NF-kappaB signaling pathway in rat vascular smooth muscle cells.

Authors: Liu, N  Liu, JT  Ji, YY  Lu, PP 
Citation: Liu N, etal., Life Sci. 2010 Sep 11;87(11-12):367-74. Epub 2010 Aug 4.
RGD ID: 5128809
Pubmed: PMID:20670634   (View Abstract at PubMed)
DOI: DOI:10.1016/j.lfs.2010.07.012   (Journal Full-text)

AIMS: C-reactive protein (CRP) plays an important role in the inflammatory process of atherosclerosis. Toll-like receptor 4 (TLR4) participates in atherogenesis by mediating the inflammatory responses. The aim of this experiment was to investigate the pro-inflammatory effects and mechanisms of CRP in rat vascular smooth muscle cells (VSMCs), especially focusing on the effects of CRP on IL-6 and peroxisome proliferator-activated receptor gamma (PPARgamma), and TLR4-dependent signal pathway. MAIN METHODS: rat VSMCs were cultured, and CRP was used as a stimulant for IL-6 and peroxisome proliferator-activated receptor gamma (PPARgamma). IL-6 level in the culture supernatant was measured by ELISA, and mRNA and protein expressions were assayed by quantitative real-time PCR and western blot, respectively. RNA interference was used to assess the roles of TLR4 and interferon regulatory factor 3 (IRF3) in the pro-inflammatory signal pathway of CRP. KEY FINDINGS: CRP stimulated IL-6 secretion, and inhibited mRNA and protein expression of PPARgamma in VSMCs in a concentration-dependent manner. Additionally, CRP induced TLR4 expression, promoted nuclear translocation of NF-kappaB (p65), and augmented IkappaBalpha phosphorylation in VSMCs. Taken together, CRP induces the inflammatory responses through increasing IL-6 generation and reducing PPARgamma expression in VSMCs, which is mediated by TLR4/IRF3/NF-kappaB signal pathway. SIGNIFICANCE: CRP is able to stimulate IL-6 production and to inhibit PPARgamma expression in VSMCs via MyD88-independent TLR4 signaling pathway (TLR4/IRF3/NF-kappaB). These provide the novel evidence for the pro-inflammatory action of CRP involved in atherogenesis.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Irf3Ratpositive regulation of canonical NF-kappaB signal transduction  IMP  RGD 
Irf3Ratpositive regulation of cytokine production  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Irf3  (interferon regulatory factor 3)


Additional Information