Yong-yi Wang

Renji Hospital, Shanghai, Shanghai Shi, China

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Publications (5)5.93 Total impact

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    ABSTRACT: End-stage renal disease (ESRD) patients are at high risk for coronary artery disease (CAD). The optimal revascularization strategy remains unknown. We performed a meta-analysis of retrospective observational trials to compare coronary artery bypass grafting (CABG) with percutaneous coronary intervention (PCI) for ESRD patients with CAD. A search of published reports was conducted to identify clinical studies comparing CABG with PCI in ESRD patients with CAD with a minimal follow-up of 12 months. Sixteen studies included 32 350 ESRD patients with revascularization. Compared with PCI, CABG was associated with a lower risk for late mortality [relative risk (RR) 0.90, 95% confidence interval (CI) 0.87-0.93], myocardial infarction event (RR 0.64, 95% CI: 0.61-0.68), repeat revascularization event (RR 0.22, 95% CI: 0.16-0.31) and cumulative events (RR 0.69, 95% CI: 0.65-0.73), despite having a higher risk for early mortality (RR 1.98, 95% CI: 1.51-2.60). In conclusion, the long-term results of PCI in ESRD patients are dismal, and CABG is significantly superior to PCI in this subset of patients.
    European journal of cardio-thoracic surgery: official journal of the European Association for Cardio-thoracic Surgery 07/2012; · 2.40 Impact Factor
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    ABSTRACT: To investigate the effect of a recombinant replication-incompetent Ad5-hGax vector on the proliferation and apoptosis of serum-induced rabbit vascular smooth muscle cells (VSMCs) in vitro, and to provide an important support that Gax would be an optimal gene for gene therapy in vein graft failure. The Ad5-hGax vector was infected into rabbit VSMCs, then the protein level of rabbit VSMCs was detected at 1 d, 3 d, 5 d by Western blot, respectively. MTT was applied to observe the inhibitory effects of overexpressed hGax on serum-induced rabbit VSMCs. the apoptosis of serum-induced rabbit VSMCs was measured by using flow cytometry in 72 h after transfection. The protein expression of human Gax in the Ad5-hGax transfected cells on 1st day, 3rd day, 5th day was determined; MTT showed that the proliferation of serum-induced rabbit VSMCs was significantly inhibited in Ad5-hGax group at 48 h, 72 h and 96 h (P<0.05, respectively); After transfecting for 72 h, flow cytometry analysis showed that the number of the apoptosis cells was increased in serum-induced Rabbit VSMCs of Ad5-hGax group (P<0.05). Overexpressed hGax could inhibit the proliferation of serum-induced Rabbit VSMCs and induce their apoptosis. These findings carry significant implications for adenovirus vector-based Gax gene therapies for vein graft failure.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 01/2012; 28(1):33-6.
  • Hui Zheng, Song Xue, Feng Lian, Yong-Yi Wang
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    ABSTRACT: Coronary artery bypass grafting using autologous saphenous veins is a standard surgical therapy for coronary artery diseases. However, post-procedure vein graft restenosis impedes its effectiveness and often leads to a high morbidity and mortality, and a reduction in the quality of life. Neointimal hyperplasia is a major cause of vein graft occlusion, and is characterized by an imbalance between vascular smooth muscle cell (VSMC) proliferation and apoptosis. So far, there have been no optimally effective pharmacological or non-pharmacological interventions for the prevention and treatment of vein graft occlusion. Gene therapy has emerged as a potential therapeutic approach, as bypass grafts can be genetically modified ex vivo prior to grafting in the coronary vasculature. Nogo-B, recognized as a vascular protective factor, has been shown to reduce neointimal thickening in graft veins, but its specific mechanism is uncertain. Evidence from diverse sources has documented that overexpressed Nogo-B can induce apoptosis of variant cancer cell lines, suggesting that overexpressed Nogo-B may have a pro-apoptotic role in VSMC. Furthermore, we have found that Nogo-B is associated with the mitogen-activated protein kinase (MAPK) signaling pathway, which plays important roles in cell growth, differentiation, and apoptosis. Recent studies have shown that VSMC apoptosis can be induced by activation of the c-Jun-N-terminal kinase (JNK)/p38 MAPK pathway. Therefore, we propose that overproduction of Nogo-B in the graft vein could result in reduced neointimal hyperplasia, the mechanism of which involves increased VSMC apoptosis induced by activation of the JNK/p38 MAPK pathway. This study will provide a new clue for gene therapy in the treatment of vein graft failure.
    Medical Hypotheses 05/2011; 77(2):278-81. · 1.18 Impact Factor
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    ABSTRACT: To investigate whether R-848 (resiquimod, toll-like receptor 7/8 agonist) can induce late preconditioning in neonatal cardiac myocytes. The protective effects of R-848 on neonatal myocytes against anoxia-reoxygenation-induced injury were tested, and intracellular reactive oxygen species (ROS) were determined. The protein synthesis inhibitor cyclohexamide (CH) and the ROS scavenger N-acetylcysteine (NAC) were used in this model to test if new protein synthesis and oxidative stress were necessary for their cardioprotective effects. The activation of nuclear factor kappa B (NFκB) and hypoxia inducible factor 1 (HIF1) was investigated by electrophoretic mobility shift assays (EMSA), and inducible nitric oxide synthase (iNOS) was assessed by immunoblotting. After iNOS was down-regulated by small interfering RNA (siRNA) transfection, the cardioprotective effect was reassessed. ROS were triggered soon after R-848 (0.01-1.0 μg/L) administration, however, the cardioprotective effect of which was induced 24 h later. This protection was abolished by CH or NAC pretreatment. NFκB and HIF1 activation and iNOS up-regulation were involved in this protective mechanism. The cardioprotective effect was also attenuated after iNOS was knocked down. R-848 provided a cardioprotective effect through a late preconditioning mechanism via a ROS/NFκB-HIF1/iNOS-dependent pathway.
    Acta Pharmacologica Sinica 05/2011; 32(5):565-72. · 2.35 Impact Factor
  • Hui Zheng, Song Xue, Feng Lian, Yong-yi Wang
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    ABSTRACT: To construct human Gax eukaryotic expression vector of pEGFP-N1-Gax, and observe its expression in the rabbit vascular smooth muscle cells(VSMCs). human Gax cDNA was obtained by polymerase chain reaction(PCR) from pCMV-SPORT6-Gax plasmid. After digested with Nhe I and Xho I, the PCR product was cloned into eukaryotic expression vector pEGFP-N1 of green fluorescent protein(GFP) reported gene encoding green fluorescence protein, and then the recombinant plasmid pEGFP-N1-Gax was transfected into rabbit VSMCs using Sofast after it was identified by restriction enzyme digestion analysis and gene sequencing. Human Gax expression in rabbit VSMCs was detected by examining GFP expression of transfected cells under fluorescence microscope and RT-PCR. Agarose gel electrophoresis detection showed that human Gax DNA segment was about 915 bp, which accorded with the expectation. The restriction enzyme digestion analysis and DNA sequencing assays of recombinant vector pEGFP-N1-Gax showed the correct orientation and sequence. The expression of GFP in rabbit VSMCs transfected with pEGFP-N1-Gax was observed by fluorescence microscopy, and the expression of human Gax mRNA was confirmed by RT-PCR. The recombinant plasmid pEGFP-N1-Gax is successfully constructed, and expressed positively in rabbit VSMCs, it provide experimental basis to study the effects of Gax gene on cardiovascular disease.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 01/2011; 27(1):29-32.