Yi-Biao Wang

Shandong University, Chi-nan-shih, Shandong Sheng, China

Are you Yi-Biao Wang?

Claim your profile

Publications (9)14.12 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of the present study was to investigate the effects of PS-341 on vascular remodeling in an experimental rat model of high blood flow-induced pulmonary arterial hypertension (PAH), as well as to elucidate its mechanisms of action. We established the PAH model by a surgical method that implanted a left-to-right shunt. Three days post-surgery, the animals were randomly assigned to 3 groups (n=15 in each group): sham-operated (control), shunt (model) and PS-341 (treated) groups. Eight weeks post-surgery, hemodynamic parameters were significantly improved in the PS-341 group compared with the shunt group (P<0.05). Immunohistochemical analysis indicated that the expression levels of ubiquitin and nuclear factor-κB (NF-κB) p65 were significantly higher in the shunt group compared with the sham-operated group (P<0.05). Semi-quantitative western blot analysis further confirmed that the levels of ubiquitin and NF-κB p65 were decreased, while those of IκB-α (an inhibitor of NF-κB) were significantly increased in the PS-341 group compared with the shunt group (P<0.05). In conclusion, PS-341 attenuates high blood flow-induced pulmonary artery remodeling in rats via inhibition of the NF-κB pathway.
    International Journal of Molecular Medicine 11/2013; 33(1). DOI:10.3892/ijmm.2013.1562 · 1.88 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: PS-341, a proteasome inhibitor, is suggested to prevent the vascular remodeling induced by high-flow pulmonary artery hypertension (PAH), but the mechanism remains unclear. The aim of the current study was to investigate the effects and possible mechanism of PS-341 on hypertension-induced vascular remodeling. Male Sprague-Dawley rats were subjected to surgical methods to produce a shunt model of PAH. Three days after the surgical procedure, the animals randomly assigned to four groups (n = 10 in each group): I: sham group; II: shunt group; III: vehicle; IV: treated group. Eight weeks postoperative, the hemodynamics data were measured through Swan-Ganz catheter; the protein expression level of proliferating cell nuclear antigen, nuclear factor-κB (NF-κB), inhibitor of nuclear factor-κB (I-κBα), transforming growth factor beta-β (TGF-β), drosophila mothers against decapentaplegic protein (Smad) and vascular endothelia growth factor (VEGF) were investigated by immunohistochemical and Western blotting; the mRNA expression level of Ubiquitin (Ub), Smad3, TGF-β1and Smad2 in lung were performed to detect by real-time reverse transcription-polymerase chain reaction analysis. The results showed that hemodynamic data and right ventricular hypertrophy were significantly improved (P < 0.05), the expression level of Ub, NF-κB, TGF-β1, Smad2 and VEGF were decreased (P < 0.05), but the level of I-κBα was increased in PS-341 treated group as compared with the shunt and vehicle groups (P < 0.05). In conclusion, the present study indicated that PS-341 could significantly improve the lung damage, attenuate pulmonary vascular remodeling induced by high blood PAH model. The mechanism may be mediated by inhibition of NF-κB and TGF-β/Smad signaling pathway and modulation the effect of VEGF.
    Clinical and Experimental Medicine 06/2013; DOI:10.1007/s10238-013-0244-7 · 2.82 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Interleukin 17 (IL-17)-producing T helper (Th17) cells and CD4(+)CD25(+) regulatory T (Treg) cells are two new T-cell subsets that are thought to be critically involved in mediating and regulating autoimmune responses. The imbalance of Th17/Treg cells has been implicated in a wide range of autoimmune disorders. The aim of our study was to determine whether the Th17/Treg balance was abnormal in children with Henoch-Schonlein Purpura (HSP). We examined twenty-three new-onset HSP patients and eighteen healthy children. The frequency of Th17 cells and the IL-17 concentration were higher in HSP patients than in healthy controls. The frequency of Treg cells and the interleukin 10 (IL-10) concentration were lower in HSP patients than in healthy controls. Compared to healthy controls, HSP patients exhibited an increase in the ratio of Th17/Treg. The Th17/Treg ratio was positively correlated with the erythrocyte sedimentation rate (ESR), kidney lesions and the clinical symptom of the presence of more than two organ systems with lesions. However, the ratio had no correlation with anti-streptolysin O (ASO) or complement 3 (C3) levels. These results indicate that a Th17/Treg imbalance exists in HSP, and it appears to be closely related to the disease onset.
    International immunopharmacology 04/2013; 16(1). DOI:10.1016/j.intimp.2013.03.027 · 2.71 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: YKL-40, a proposed marker of inflammation and endothelial dysfunction, is associated with atherosclerosis and an increased cardiovascular mortality in the general population. However, the relationship between YKL-40 and arterial stiffness in hypertensive patients has not been adequately assessed. The relationship between serum levels of YKL-40 and arterial stiffness was evaluated in 93 essential hypertensive subjects and 80 normal subjects. Essential hypertensive subjects were divided into two groups based upon urinary albumin-to-creatinine ratio (ACR): nonmicroalbuminuric group, (ACR <30 mg/g, n = 50) and microalbuminuric group (ACR ≥30 mg/g, n = 43). Large artery wall stiffness was assessed by measuring femoral arterial stiffness and carotid-femoral pulse wave velocity (cf-PWV). Serum levels of YKL-40 were determined by enzyme-linked immunosorbent assay (ELISA). The study demonstrated that YKL-40,cf-PWV and femoral arterial stiffness were increased significantly (P<0.05) in the hypertensive group compared with normal controls. These measurements were also increased significantly ( P<0.05) in the microalbuminuric group compared with the nonmicroalbuminuric group. YKL-40 was positively correlated with cf-PWV( r = 0.44, P = 0.000) and femoral arterial stiffness ( r = 0.42, P =0.001). Multiple linear stepwise regression analysis showed that YKL-40 was the impact factor of arterial stiffness ( P<0.05). YKL-40 levels are elevated in essential hypertension subjects with an independent association between increasing YKL-40 levels and increasing arterial stiffness. The study suggests it played a positive role of YKL-40 in the progressing vascular complications in patients with essential hypertension.
    BMC Cardiovascular Disorders 05/2012; 12:35. DOI:10.1186/1471-2261-12-35 · 1.50 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: We investigated the safety and feasibility of intratracheal administration of autologous bone marrow-derived mononuclear cells (ABM-MNCs) and observed the effects in a canine model of pulmonary hypertension (PH). The PH model was induced by intravenous injection of 3mg/kg dehydromonocrotaline (DMCT) via the right atrium. Two weeks after DMCT administration, the animals received 4 different treatments (n=10 in each group): (I) negative control group; (II): ABM-MNCs group; (III) PH group; (IV) PH+ABM-MNCs group. Six weeks after injection of cells (10⁷), the hemodynamic data were significantly improved in group IV compared with group III (P<0.05). The ratio of right ventricular weight to left ventricular plus septal weight was significantly decreased in group IV compared with group III (P<0.05). The mRNA levels of vascular endothelial growth factor, preproendothelin-1, interleukin-6 and tumor necrosis factor-α were significantly improved in group IV compared with group III (P<0.05). The immunofluorescence result showed that 6 weeks after administration ABM-MNCs could differentiate into pulmonary vascular endothelial cells. Six weeks after intratracheal administration, ABM-MNCs significantly improved the impairment caused by DMCT in a canine model of PH (ie, decreased pulmonary arteriolar narrowing, alveolar septum thickening and right ventricular hypertrophy, enhanced angiogenesis) and this provides a firm foundation for a clinical trial.
    Circulation Journal 01/2012; 76(4):977-85. DOI:10.1253/circj.CJ-11-1175 · 3.69 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pulmonary hypertension (PH) is a rapidly progressive and fatal disease. In recent years, despite drug treatment made significant progress, the prognosis of patients with advanced PH remains extremely poor. The authors implanted bone marrow-derived mesenchymal stem cells (BMSCs) intravenously into the PH model rats and observed the effect of MSCs on right ventricular (RV) impairments. BMSCs were isolated, cultured from bone marrow of rats and stained with the cross-linkable membrane dye in vitro. One week after, a PH model was induced by subcutaneous injection of monocrotaline, the animals were randomly divided into 4 groups (n = 20 in each group): I, control; II, MSCs implantation; III, PH and IV, PH + MSCs implantation. Two weeks after MSCs implantation, the authors observed the MSC survival and transformation by immunofluorescence microscopy. On the other hand, RV hypertrophy and the elevation of systolic pressure were detected by echocardiography. Three weeks after monocrotaline injection, RV systolic pressure, mean right ventricular pressure and mean pulmonary arterial pressure were significantly elevated in group III than in group I and II (P < 0.05) but significantly lower in group IV than in group III (P < 0.05). These results showed that implantation of MSCs could improve RV impairments caused by experimental PH. Histochemical results confirmed that transplanted MSCs were still alive after 2 weeks and part of the cells could differentiate into pulmonary vascular endothelial cells. Intravenous implantation of MSCs could significantly reduce or even reverse the progression of MCT-induced PH, improve cardiac function and hemodynamics.
    The American Journal of the Medical Sciences 08/2011; 343(5):402-6. DOI:10.1097/MAJ.0b013e31822dc5d3 · 1.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The present study was designed to investigate the influence of Congenital Heart Disease (CHD) on the mentality and behavior in children, and to compare post operative mentality and behavior in children receiving interventional therapy and congenital heart surgery. Mentality and behavior of 232 children suffering from CHD were examined with Achenbach Child Behavior Checklist (CBCL) edited by XU Tao-yuan in 1992 and 100 sex, age, education and achievement-matched children with pneumonia were enrolled as controls. The mentality and behavior abnormal rates of the boys and girls suffering from CHD were significantly higher than those of controls (P < 0.01, P < 0.05). The behavior abnormities of the boys presented as depression, social flinch, physical complains, assault and violate rules. Whereas the girls presented as depression, social flinch, physical complains and violate rules. The total cursory mark of postoperative check result of the interventional and surgical children, both in girls and in boys, were significantly lower than those of the preoperative children (P < 0.05). The total and assault cursory mark of postoperative check result of children treated with interventional therapy were significantly lower than those of children treated with the surgical operations (P < 0.05). The abnormal rates of mentality and behavior positively correlated with the disease course. CHD is associated with increased abnormal mentality and behavior of the children. Early treatment, especially the interventional therapy can significantly improve the mentality and behavior of the children with CHD.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2008; 36(5):418-21.
  • [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the feasibility of transferring p21 gene into lung tissue with recombinant adenovirus with full-length cDNA of p21 inserted in the Wistar rat model of pulmonary hypertension (PAH) induced by left-to-right shunt, study the expression of the desired gene in vivo, find if overexpression of desired gene can inhibit pulmonary hypertension. With full-length cDNA of p21 transfected HEK293 cells with clonfectin, and was packed, amplified in order to obtain the high-titer recombinant adenovirus (AdCMV-p21). The infection titer was determined by TCID50 method and was diluted into 1.67 x 10(8) pfu/L. Wistar rats were randomly allocated to control group (n = 10), model group (n = 15), test group (n = 10) and test control group (n = 10). In model group and test group left-to-right shunt pulmonary hypertension was developed by using cuff technique. AdCMV-p21 was transfected into test group and test control group using tracheal inhalation. The mPAP, mRVP and RVHI were measured and compared between every two groups. The left lung was immunohistochemically stained to observe the result of transfection. The right lung was HE stained to observe morphological changes in arteria pulmonalis and calculate WT%. The mRVP, mPAP and WT% in model group and test group were significantly higher than those in control (P < 0.05), which suggested that the rat model of PAH was established successfully. Brown spots in the nucleus of VSMCs of pulmonary artery were seen in test group and test control group, which indicated that AdCMV-p21 was transfected successfully. The rate of transfected cells in test group was (42.8 +/- 11.6)%, which was equal to that of test control group (P > 0.05). In test group, the mPAP was (20.06 +/- 3.40) mm Hg (1 mm Hg = 0.133 kPa), mRVP was (22.53 +/- 2.53) mm Hg, WT% was (30.8 +/- 3.5)%, which were significantly lower than those in model group (P < 0.05), but higher than those in control group and test control group (P < 0.05). The recombinant adenovirus could successfully carry p21 and transfect the lung tissue of PAH rat model, and full expression of p21. p21 gene could inhibit the development of PAH.
    Zhonghua er ke za zhi. Chinese journal of pediatrics 02/2008; 46(2):139-42.
  • [Show abstract] [Hide abstract]
    ABSTRACT: This study was designed to investigate the pathophysiological role of adrenomedullin (ADM) in congenital heart disease. Forty-eight children with congenital heart disease confirmed by cardiac echocardiography and catheterization were studied. The patients were divided into three groups on the basis of hemodynamic indices measured during cardiac catheterization: high pulmonary blood flow with (group 1) or without (group 2) pulmonary hypertension (mean pulmonary arterial pressure > 20 mmHg) and a cyanosis group (without high pulmonary blood flow) (group 3). Six children who recovered from Kawasaki disease were used as a Control group. Plasma ADM levels were measured by radioimmunoassay. The plasma ADM levels from the femoral vein were significantly higher than those from femoral artery in patients with congenital heart disease. The patients from group 1 and group 3 had higher plasma ADM levels (1.9 +/- 1.8 pmol/L and 2.4 +/- 1.3 pmol/L, respectively) than the controls (1.0 +/- 1.4 pmol/L; P < 0.01). Plasma ADM levels were significantly negatively correlated with mean systemic arterial pressure, oxygen saturation in mixed vein and oxygen saturation in systemic artery (r=-0.401, -0.562, -0.600, respectively; P < 0.01) but positively correlated with pulmonary vascular resistance (r=0.406; P < 0.01). Plasma ADM levels are increased in congenital heart disease with high pulmonary blood flow and hypertension or with cyanosis. Plasma ADM levels are related to pulmonary arterial resistance and hypoxemia. Increased ADM levels may play roles in reducing the pulmonary arterial resistance and alleviating hypoxemia in these patients.
    Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 05/2006; 8(2):90-2.