Peipei Lu

Publications (3)7.09 Total impact

• Article: C-reactive protein induces TNF-α secretion by p38 MAPK-TLR4 signal pathway in rat vascular smooth muscle cells.

  Na Liu, Juntian Liu, Yuanyuan Ji, Peipei Lu, Chenjing Wang, Fang Guo
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  ABSTRACT: Atherosclerosis is a chronic inflammatory disease. C-reactive protein (CRP) not only is an inflammatory marker but also regulates the expressions of other inflammatory cytokines associated with the pathogenesis of atherosclerosis. Toll-like receptor 4 (TLR4) also contributes to atherogenesis via transducting inflammatory signals. Herein, our studies focused on characterizing the effect of CRP on tumor necrosis factor α (TNF-α) production and TLR4-related molecular mechanisms in rat vascular smooth muscle cells (VSMCs). The results showed that CRP stimulated VSMCs to secrete TNF-α and enhanced TLR4 expression in a time-concentration-dependent manner. TLR4 knockdown significantly inhibited CRP-induced TNF-α generation, and p38 mitogen-activated protein kinase (MAPK) blocker SB203580 depressed TLR4 expression and TNF-α production initiated by CRP in VSMCs. The data demonstrate that CRP triggers an inflammatory response in rat VSMCs by inducing TNF-α secretion, which is mediated by p38 MAPK-TLR4 signaling pathway.
  Inflammation 08/2011; 34(4):283-90. · 1.75 Impact Factor
• Article: Toll-like receptor 4 signaling mediates inflammatory activation induced by C-reactive protein in vascular smooth muscle cells.

  Na Liu, Juntian Liu, Yuanyuan Ji, Peipei Lu
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  ABSTRACT: C-reactive protein (CRP) is considered to induce the inflammatory response during atherosclerosis. Toll-like receptor 4 (TLR4)-mediated inflammatory signaling has been shown to facilitate atherogenesis. It remains thoroughly unknown whether TLR4 mediates the proinflammatory effect of CRP. Thus, the study was designed to explore TLR4-related mechanism of proinflammatory effect of CRP in rat vascular smooth muscle cells (VSMCs). CRP increased mRNA levels and protein expressions of vascular endothelial growth factor A (VEGF-A) and inducible nitric oxide synthase (iNOS) in VSMCs, and enhanced NO secretion in the medium. But, CRP hindered nuclear translocation of glucocorticoid receptor (GR) and decreased mRNA level and protein phosphorylation of GR in VSMCs. TLR4 small-interfering RNA (siRNA) significantly reversed the effects of CRP. These suggest that CRP is able to induce inflammatory responses via TLR4 in VSMCs. More importantly, our data provide novel evidence that CRP exerts a proinflammatory action via TLR4-dependent signaling pathway (AT(1)R-p38 MAPK-TLR4-PKCalpha) in VSMCs.
  Cellular Physiology and Biochemistry 01/2010; 25(4-5):467-76. · 2.86 Impact Factor
• Article: Fibrinogen, fibrin, and FDP induce C-reactive protein generation in rat vascular smooth muscle cells: pro-inflammatory effect on atherosclerosis.

  Fang Guo, Juntian Liu, Chenjing Wang, Na Liu, Peipei Lu
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  ABSTRACT: Atherosclerosis is a chronic inflammatory disease in the vessel. As an inflammatory cytokine, C-reactive protein (CRP) participates in the pathogenesis of atherosclerosis through multiple bioactivities. It has been widely accepted that hyperfibrinogenemia is associated with the formation and progression of atherosclerosis. But, it is unknown whether fibrinogen exerts a pro-inflammatory effect on vascular smooth muscle cells (VSMCs). The purpose of the present study was to observe the effect of fibrinogen, fibrin, and fibrin degradation products (FDP) on CRP generation in VSMCs. CRP mRNA expression was identified with the reverse transcription polymerase chain reaction. CRP level in the supernatant of VSMCs was measured with the enzyme-linked immunosorbent assay. CRP expression in VSMCs was examined with the immunocytochemical method. The results showed that fibrinogen, fibrin, and FDP all induced CRP production in VSMCs both in mRNA level and in protein level in a time- and concentration-dependent manner. The potency is FDP>fibrin>fibrinogen, which seems to mean that their pro-inflammatory activity decreases with increase of molecular weight of these three proteins. The finding provides a new mechanism for atherogenic effect of fibrin(ogen) and FDP, and emphasizes the importance of therapy of hyperfibrinogenemia in atherosclerosis.
  Biochemical and Biophysical Research Communications 10/2009; 390(3):942-6. · 2.48 Impact Factor