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Publications (9)36.36 Total impact

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    ABSTRACT: An increasing amount of evidence shows that the OX40-OX40L interaction serves an important function in atherosclerosis. However, the mechanism of the OX40 signaling pathway remains unclear. This study investigates the effect of OX40-OX40L interaction on the levels of intracellular reactive oxygen species (ROS) and the secretion of Cyclophilin A (CyPA) in C57BL/6J mice atherogenesis.
    International journal of cardiology. 08/2014;
  • International journal of cardiology 01/2014; · 6.18 Impact Factor
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    ABSTRACT: Our previous studies showed that increased levels of cyclophilin A (CyPA) may be a valuable marker for predicting the severity of acute coronary syndromes and that interruption of CD137-CD137L interactions diminished the formation and progression of atherosclerosis in apolipoprotein E-deficient (ApoE-/-) mice. Here, we sought to determine whether the proinflammatory factor CyPA is involved in atherosclerosis regulated by CD137-CD137L interactions. A constrictive collar was placed around the right carotid arteries of ApoE-/- mice that were fed a high-fat diet to induce atherosclerotic plaque formation. After that, the mice were intraperitoneally injected with anti-CD137 or anti-CD137L in the presence or absence of the recombinant lentiviral vectors LVTHM-CyPA or pGC-FU-CyPA, respectively. Interestingly, activation of CD137-CD137L was negatively correlated with CyPA expression in vivo and in vitro. Stimulating CD137-CD137L interaction significantly increased CyPA, which was concurrent with the upregulation of proinflammatory cytokines, chemokines and matrix metalloproteinases and resulted in the promotion of atherosclerosis in ApoE-/- mice. Silencing CyPA could eliminate these effects, and restoration of CyPA effectively and consistently attenuated the atherosclerotic suppression phenotypes elicited by the blockade of CD137-CD137L. These observations suggest that CD137-CD137L interactions mediated via regulation of CyPA contribute to the progression of atherosclerosis.
    PLoS ONE 01/2014; 9(2):e88563. · 3.53 Impact Factor
  • International journal of cardiology 10/2013; · 6.18 Impact Factor
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    ABSTRACT: We previously reported the emerging role of CD137-CD137L interaction in inflammation and atherosclerosis. The mechanism of CD137-CD137L interaction may be related to a variety of signaling pathways. The most important signaling pathway involves the activation of phospholipase C(PLC) which induces the diacylglycerol-protein kinase C(DAG-PKC) and the inositol trisphosphate-intracellular free calcium((IP3-[Ca(2+)]i) pathway. In the current study, we investigated whether CD137-CD137L interaction can stimulate the PLC signaling pathway in human umbilical vein endothelial cells (HUVEC). The diacylglycerol (DAG) and inositol trisphosphate (IP3) levels in HUVEC were measured by radioenzymatic assay. The activity of protein kinase (PKC) was detected by its ability to transfer phosphate from [γ-(32)P]ATP to lysine-rich histone. The [Ca(2+)]i concentrations were measured by flow cytometric analysis. The DAG level and PKC activity were increased in a concentration-dependent, biphasic manner in HUVEC induced by anti-CD137. PKC activity was mainly in the cytosol at rest, and then translocated to the membrane when stimulated by anti-CD137. Similarly, rapid IP3 formation induced by anti-CD137 coincided with the peak of the DAG level. Moreover, anti-CD137 induced peak [Ca(2+)]i responses including the rapid transient phase and the sustained phase. However, anti-CD137L suppressed the activation of the DAG-PKC and IP(3)-[Ca(2+)]i signaling pathway, which was stimulated by anti-CD137 in HUVEC. In conclusion, the data suggested that CD137-CD137L interaction induces robust activation of the PLC signaling pathway in HUVEC.
    Chemico-biological interactions 09/2013; · 2.46 Impact Factor
  • International journal of cardiology 07/2013; · 6.18 Impact Factor
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    ABSTRACT: Our previous study has demonstrated that the Toll-like receptor 4 (TLR4) signaling pathways contribute to the induction of tissue factor (TF) expression by anti-β(2)-glycoprotein I/β(2)-glycoprotein I (anti-β(2)GPI/β(2)GPI) in human acute monocytic leukemia cell line THP-1. In this study, we focused on the identification of the downstream targets of the TLR4 pathways. When THP-1 cells were treated with anti-β(2)GPI/β(2)GPI complex, enhanced TF expression was observed, along with induced phosphorylation of p38, ERK1/2 and JNK1/2 MAPKs. When the activity of MAPKs was blocked by their corresponding inhibitors (SB203580: p38; U0126: ERK; SP600125: JNK), the expression of TF was reduced significantly. Furthermore, the anti-β(2)GPI/β(2)GPI-induced phosphorylation of p38, ERK1/2 and JNK1/2 was inhibited significantly by TAK-242, a blocker of the signaling transduction mediated by the intracellular domain of TLR4; sc-204013, a specific inhibitor of IRAKs, was also able to partially inhibit the phosphorylation of the MAPKs. Our results demonstrated that MAPKs (p38, ERK1/2 and JNK1/2) were the crucial downstream targets of the anti-β(2)GPI/β(2)GPI-triggered TLR4 signaling pathways in THP-1 cells. This essential role of MAPKs may also promote better understanding of the pathogenesis of antiphospholipid syndrome (APS).
    Thrombosis Research 08/2012; 130(4):e229-35. · 3.13 Impact Factor
  • International journal of cardiology 03/2012; 157(1):134-7. · 6.18 Impact Factor
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    ABSTRACT: Cyclophilin A is a secreted molecule that has a physiological and pathological role in cardiovascular diseases. However, limited information is available on the relationship between cyclophilin A concentration and acute coronary syndromes (ACS). We investigated whether cyclophilin A concentration is related to the stability of coronary atherosclerotic plaque in patients with ACS. This study included normal controls (n=50), patients with stable angina (SA) (n=60) and patients with ACS, including unstable angina (UA) (n=60) and acute myocardial infarction (AMI) (n=90). Serum soluble cyclophilin A, matrix metalloproteinase 9 (MMP-9), MMP-3 and C-reactive protein concentrations (CRP) were measured. All coronary stenosis were assessed by angiographic coronary stenosis morphology. Serum cyclophilin A concentration in ACS (UA and AMI ) subjects were significantly higher than those in patients with SA and controls (p<0.05). Serum cyclophilin A correlated positively with serum MMP-3 and MMP-9 and CRP in ACS patients(r(1)=0.69, r(2)=0.52, r(3)=0.49 p<0.0001), but not in control. Furthermore, the increased cyclophilin A concentrations was associated with the number of complex coronary stenoses (r(1)=0.63, p<0.0001), but not smooth lesions or stenosis severity, in coronary artery disease patients. Logistic regression analysis also demonstrated that serum cyclophilin A concentration was an independent predictor factor for ACS( OR, 2.721, 95% CI 1.563-4.042, p=0.001). Patients with ACS showed that increased concentrations of cyclophilin A may be a valuable marker for predicting the severity of ACS.
    Clinica chimica acta; international journal of clinical chemistry 12/2011; 413(7-8):691-5. · 2.54 Impact Factor