Wei Yuan

Jiangsu University, Chenkiang, Jiangsu Sheng, China

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Publications (14)54.33 Total impact

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    ABSTRACT: Objective: To evaluate the effect of new regional cooperative rescue model on the first medical contact-to-balloon time and outcome in patients with ST-elevation myocardial infarction. Method: Patients with acute myocardial infraction (AMI) and onset time within 24 hours transferred from other hospitals to our clinic and underwent emergent percutaneous coronary intervention (PCI) between January 2010 and January 2013 were included in this study. Patients were divided into two groups: regional cooperative treatment group (n = 230) and control group (n = 168) according to whether the first contact clinic belongs to the regional cooperative rescue model or not. The first medical contact to balloon (FMC-to-B) time, door to balloon (D-to-B) time, referral time, cardiac function, mean cost, days of hospitalization, and major adverse cardiac event (MACE) during the 6 months follow up were compared. Results: Mean FMC-to-B time, D-to-B time and referral time were significantly decreased from (212 ± 37), (107 ± 18), (103 ± 23) min (control group) to (98 ± 23), (25 ± 7), (62 ± 12) min respectively in regional cooperative treatment group. Mean medical cost (42 221 (23 184, 77 768) RMB vs. 49 654 (25 126, 122 433) RMB) and days of hospitalization (7 (5, 13) days vs. 10 (6, 20) days) were also significantly lower in regional cooperative treatment group than in control group. At 6 months follow up, LVEF was significantly higher(54.9% ± 8.6% vs. 48.9% ± 9.1%, P = 0.01), LVEDD ((48.9 ± 5.7)mm vs.(51.4 ± 6.0) mm, P < 0.01) as well as MACE rate (7.4% (17/230) vs. 17.9% (30/168) , P < 0.05) were significantly lower in regional cooperative treatment group than in control group. Conclusion: The regional cooperative rescue model can decrease the FMC-to-B time, improve cardiac function, and reduce both patients' financial burden and MACE in patients with acute myocardial infarction.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 08/2014; 42(8):646-9. DOI:10.3760/cma.j.issn.0253-3758.2014.08.007
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    ABSTRACT: Background: 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. Methods: The atherosclerotic plaque model was established by placing a rapid perivascular carotid collar on C57BL/6J mice fed with a western-type diet. In vivo, the expressions of CyPA in mouse plaque and lymphocytes were detected by immunohistochemical and Western blot analyses, respectively. In vitro, the expression of CyPA protein in cultured lymphocytes of C57BL/6J mice was assessed by using Western blot analysis. The level of ROS was detected through flow cytometry. Results: CyPA expression was significantly increased in the atherosclerotic lesions and lymphocytes from C57BL/6J mice. The ROS levels in OX40(+)-lymphocytes were increased in vitro and in vivo. After stimulating the OX40-OX40L interaction, the ROS and CyPA levels in lymphocytes were obviously increased in vitro, whereas anti-OX40L mAb significantly down-regulated the anti-OX40 mAb-induced ROS generation and inhibited CyPA secretion in lymphocytes. Conclusion: The OX40-OX40L interaction up-regulates intracellular levels of ROS in C57BL/6J mice and increases CyPA secretion in lymphocytes. Increased CyPA secretion may serve an important function in atherosclerotic plaque formation.
    International Journal of Cardiology 08/2014; 176(2). DOI:10.1016/j.ijcard.2014.07.111 · 4.04 Impact Factor
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    ABSTRACT: Objective: The aim of this study was to determine whether inhibition of cyclophilin A by lentivirus-mediated RNA interference (RNAi) could inhibit progression of atherosclerotic plaques and increase collagen production. Methods: Atherosclerostic plaque model was induced by rapid perivascular carotid silicone collar placement in ApoE(-/-) mice. The recombinant CyPA-RNAi-Lentivirus (CyPA-RNAi-LV) or negative control-green fluorescent protein-Lentivirus (NC-GFP-LV) were constructed and transfected into right carotid plaques, respectively. Using the local injection method, ApoE(-/-) mice carotid artery plaque were intervened 10 min in the silicone collar placement with 10 µl (1.0 × 10⁸ TU/ml) lentivirus vector. The areas and CyPA expression of plaques were analyzed by morphological observation, real-time polymerase chain reaction (RT-PCR) and Western blot respectively. Results: CyPA-RNAi-LV not only prevented plaques progression ((9 085 ± 671) µm² to (18 021 ± 1 901) µm²), but also decreased plaque lipid content ((28.9 ± 6.3)% to (17.8 ± 4.5)%), increased plaque collagen content ((24.2 ± 4.8)% to (35.1 ± 5.2)%) at 6 weeks after lentivirus transfection. The intima/media ratio (0.36 ± 0.11 vs. 0.65 ± 0.12, P < 0.05) and degree of lumen stenosis (intima/lumen ratios, 0.18 ± 0.02 vs. 0.33 ± 0.03, P < 0.05) were also significantly reduced by CyPA-RNAi-LV. Moreover, RT-PCR analysis revealed downregulated expressions of proinflammatory cytokines and matrix metalloproteinases (MMP-9 -17.5%) in the CyPA-RNAi-LV group. Conclusion: Lentivirus-mediated CyPA silencing by siRNA could inhibit plaques progression and reduce local inflammation through the anti-inflammatory effects in this model.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 07/2014; 42(7):593-7. DOI:10.3760/cma.j.issn.0253-3758.2014.07.014
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    ABSTRACT: Objective: To investigate the association between CD147 expression and its untranslated regions 3'UTR rs8259 T/A polymorphism and acute coronary syndrome (ACS). Methods: The genotypes of CD147 were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods in 182 ACS patients and 328 healthy controls. The plasma level of CD147 was determined by enzyme-linked immunosorbent assay (ELISA). CD147 mRNA and protein expression was detected by real-time fluorescent quantitative PCR (RT-qPCR) and Western blot. Results: The plasma CD147 level obtained from radial artery in ACS patients ((3.63 ± 0.70) pg/L) was significantly higher than in control ((2.45 ± 0.27) pg/L, P < 0.05), and highest in plasma obtained from the coronary artery ((4.28 ± 1.03) pg/L, P < 0.05) in ACS patients. Furthermore, the plasma CD147 level was higher in the ACS patients with rs8259 AA genotype than in the ACS patients with rs8259 TT genotype ((4.08 ± 0.41) pg/L vs. (3.05 ± 0.79) pg/L in radial artery and (5.29 ± 0.62) pg/L vs. (3.13 ± 0.52) pg/L in coronary artery, both P < 0.05). There are an enhanced expression of CD147 mRNA (2.45 times higher than control) and protein (3.66 ± 1.56 vs. 1.81 ± 1.29) in PBMCs from ACS patients than that from controls (both P < 0.05). The PBMCs CD147 mRNA and protein expression level were significantly higher in ACS patients with rs8259 AA genotype (mRNA:2.45 ± 0.35, protein:1.63 ± 0.16) compared to ACS patients with rs8259 TT genotype (mRNA:1.69 ± 0.15, protein: 0.88 ± 0.16, both P < 0.05). Multiple logistic analysis showed that CD147 T allele (AT+TT) was a protective factor to ACS (OR = 0.667, 95% CI 0.507-0.879, P < 0.05). Conclusions: The over-expression of CD147 is involved in the pathogenesis of ACS. The CD147 3'UTR rs8259 T allele may be a protective factor for ACS, its polymorphism can affect the CD147 protein expression in ACS patients.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 07/2014; 42(7):566-70.
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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 02/2014; 9(2):e88563. DOI:10.1371/journal.pone.0088563 · 3.23 Impact Factor
  • International journal of cardiology 01/2014; 172(3). DOI:10.1016/j.ijcard.2014.01.031 · 4.04 Impact Factor
  • International journal of cardiology 10/2013; 169(5). DOI:10.1016/j.ijcard.2013.10.039 · 4.04 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; 206(2). DOI:10.1016/j.cbi.2013.09.014 · 2.58 Impact Factor
  • International journal of cardiology 07/2013; 168(2). DOI:10.1016/j.ijcard.2013.07.060 · 4.04 Impact Factor
  • Heart (British Cardiac Society) 10/2012; 98(Suppl 2):E54-E54. DOI:10.1136/heartjnl-2012-302920a.132 · 5.60 Impact Factor
  • 23rd Great Wall International Congress of Cardiology/Asia Pacific Heart; 10/2012
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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. DOI:10.1016/j.thromres.2012.08.303 · 2.45 Impact Factor
  • International journal of cardiology 03/2012; 157(1):134-7. DOI:10.1016/j.ijcard.2012.03.039 · 4.04 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. DOI:10.1016/j.cca.2011.12.009 · 2.82 Impact Factor