Xian-Mei Wang

Chengdu Military General Hospital, Hua-yang, Sichuan, China

Are you Xian-Mei Wang?

Claim your profile

Publications (11)14.95 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Myocardial necrosis after ST-segment elevation myocardial infarction (STEMI) can cause left ventricular systolic dysfunction, which has been associated with poor outcomes. Some authors have reported that women have higher mortality rates after primary percutaneous coronary intervention (PCI), but differences between the sexes with regard to recovery of ejection fraction (EF) in patients with STEMI receiving primary PCI have not been evaluated. We aimed to assess the effect of sex on EF recovery in patients with anterior wall STEMI after primary PCI. A total of 202 consecutive patients (134 men) admitted due to anterior wall STEMI to our hospital over 44 months were evaluated. All patients were taken directly to the Cardiac Catheterization Laboratory for primary PCI. Baseline clinical variables were collected, and left ventricular ejection fraction (LVEF) was measured by echocardiography using the biplane Simpson model on the day after PCI and 6 months later. Women were significantly older than men (66.9±8.5 vs. 59.5±9.8, P<0.001). They also had a higher prevalence of hypertension and were less likely to be smokers compared with men. The time from symptom onset to hospital admission was longer in women than in men (8.9±3.0 vs. 7.8±2.4 h, P=0.048). At 1 day and 6 months after PCI, the EF was lower in women compared with men. The difference in values between 1 day and 6 months after PCI was also significantly lower in women compared with men (3.0±2.3 vs. 5.8±3.7, P<0.001). Multivariable linear regression analyses showed that being female was a significant predictor of LVEF recovery, even after adjustment for important clinical covariates. These data suggest that being female is an independent determinant of LVEF recovery in patients with anterior myocardial infarction after primary PCI.
    No preview · Article · Nov 2013 · Coronary artery disease
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Extracellular matrix metalloproteinase inducer (EMMPRIN), a 58-kDa cell surface glycoprotein, has been identified as a key receptor for transmitting cellular signals mediating metalloproteinase activities, as well as inflammation and oxidative stress. Clinical evidence has revealed that EMMPRIN is expressed in human atherosclerotic plaque; however, the relationship between EMMPRIN and atherosclerosis is unclear. To evaluate the functional role of EMMPRIN in atherosclerosis, we treated apolipoprotein E-deficient (ApoE(-/-)) mice with an EMMPRIN function-blocking antibody. Methods and results: EMMPRIN was found to be up-regulated in ApoE(-/-) mice fed a 12-week high-fat diet in contrast to 12 weeks of normal diet. Administration of a function-blocking EMMPRIN antibody (100 μg, twice per week for 4 weeks) to ApoE(-/-) mice, starting after 12 weeks of high-fat diet feeding caused attenuated and more stable atherosclerotic lesions, less reactive oxygen stress generation on plaque, as well as down-regulation of circulating interleukin-6 and monocyte chemotactic protein-1 in ApoE(-/-) mice. The benefit of EMMPRIN functional blockage was associated with reduced metalloproteinases proteolytic activity, which delayed the circulating monocyte transmigrating into atherosclerotic lesions. Conclusion: EMMPRIN antibody intervention ameliorated atherosclerosis in ApoE(-/-) mice by the down-regulation of metalloproteinase activity, suggesting that EMMPRIN may be a viable therapeutic target in atherosclerosis.
    No preview · Article · May 2013 · International journal of cardiology
  • [Show abstract] [Hide abstract]
    ABSTRACT: To explore the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in THP-1 macrophages induced by angiotensin II (Ang II) and the mechanism of EMMPRIN expression. THP-1 cells were cultured and induced into macrophages, then stimulated with 10(-6) mol/L Ang II. Levels of EMMPRIN gene and its protein were measured by real-time polymerase chain reaction and western blotting. Prostaglandin E(2) (PGE(2)) expression was assayed by enzyme-linked immunosorbent assay. Antagonists of the angiotensin type-1 receptor (AT(1)R) and angiotensin type-2 receptor (AT(2)R) were used to inhibit the effect of Ang II, and PGE(2) added to detail the mechanism of Ang II-induced EMMPRIN expression. Ang II clearly induced the expression of EMMPRIN mRNA and protein in macrophages; this expression peaked at 12 h and declined after 24 h. The tendency of enhancement of the levels of cyclooxygenase-2 (COX-2) and PGE(2) was coincident with EMMPRIN expression. AT(1)-receptor antagonists and COX-2 inhibitors inhibited the effect of Ang II, but AT(2)-receptor antagonists did not. Ang II can up-regulate EMMPRIN expression in THP-1 macrophages via the AT(1)/COX-2/PGE(2) signal transduction pathway, and the effect can be inhibited by losartan and NS-398.
    No preview · Article · Dec 2010 · Agents and Actions
  • [Show abstract] [Hide abstract]
    ABSTRACT: Recent studies on atherosclerosis showed that an inducer of MMPs, EMMPRIN, is highly expressed in human atheromas. This suggested the important role of EMMPRIN in the stability of atherosclerotic plaques. Angiotensin II, one of the main functional peptides in the renin-angiotensin system, is involved in the advancement of atherosclerosis. We evaluated the effect of angiotensin II on EMMPRIN expression in THP-1 macrophages, and postulated the potential mechanisms underlying its effects. We established THP-1 macrophages using PMA. The effect of angII on EMMPRIN expression in THP-1 macrophages was then investigated. Results from analyses of RT-PCR and western blotting showed that angII could upregulate EMMPRIN expression. This was mediated via the AT1R, but not the AT2R. The NF-kappaB inhibitor PDTC and P65 RNAi treatment could suppress the effect of angII on EMMPRIN, suggesting the involvement of the NF-kappaB pathway. A gelatin zymography assay showed that MMP-9 activity was related to EMMPRIN expression. AngII upregulates the expression of EMMPRIN. NF-kappaB is the critical factor involved in the upregulation of EMMPRIN induced by angII.
    No preview · Article · May 2010 · Regulatory Peptides
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Endothelial dysfunction is associated with cardiovascular diseases. The Ca2+ influx occurring via activation of plasmalemma Ca2+ channels was shown to be critical in signaling the increase in endothelial permeability in response to a variety of permeability-increasing mediators. It has been reported that angiotensin II (AngII) could induce Ca2+ signaling in some cells, and transient receptor potential canonical 1 (TRPC1) had an important role in this process. The objective of this study was to examine the mechanism of AngII-induced Ca2+ entry and vascular endothelial hyperpermeability. Human umbilical vein endothelial cells (HUVECs) exposed to AngII exhibited dose-dependent increase in [Ca2+]i and endothelial permeability. Quantitative real-time RT-PCR and Western blotting showed that the level of TRPC1 expression had increased significantly at 12h and at 24h after treatment of HUEVCs with AngII. The expression of p65 was suppressed using an RNAi strategy. The results showed that the NF-κB signaling pathway and type-1 receptor of AngII was involved in AngII-induced TRPC1 upregulation. Moreover, knockdown of TRPC1 and NF-κB expression attenuates AngII-induced [Ca2+]i and endothelial permeability. NF-κB and TRPC1 have critical roles in AngII-induced Ca2+ entry and endothelial permeability.
    Preview · Article · Jul 2009 · Peptides
  • [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the relationship between the plasma macrophage migration inhibitory factor (MIF), activator protein-1 (AP-1) and MMP-9 concentrations and the severity of coronary artery lesions in coronary heart disease (CHD) patients. Patients were divided into normal controls (n = 35), stable angina pectoris (SAP, n = 32) and acute coronary syndrome (ACS, n = 75) according to the coronary angiography (CAG), clinical and laboratory examinations. The CAG severity and extent of coronary lesions were analyzed by means of Gensini coronary score system. Enzyme linked immunosorent assay was used to measure the plasma MIF, AP-1 and MMP-9 concentrations. Plasma MIF, AP-1 and MMP-9 concentrations were significant increased in CHD patients [MIF: (14.97 +/- 2.11) microg/L, AP-1: 1.43 +/- 0.33, MMP-9: (1.48 +/- 0.14) microg/L] compared to those in control group [MIF: (9.07 +/- 1.28) microg/L, AP-1: 0.71 +/- 0.13, MMP-9: (1.01 +/- 0.07) microg/L, all P < 0.05]. The MIF, AP-1 and MMP-9 concentrations in ACS group [MIF: (16.66 +/- 2.56) microg/L, AP-1: 1.56 +/- 0.22, MMP-9: (1.58 +/- 0.14) microg/L] were also significant higher than those in SAP group [MIF: (11.01 +/- 2.12) microg/L, AP-1: 1.04 +/- 0.25, MMP-9: (1.25 +/- 0.07) microg/L, all P < 0.05] and there was significant positive correlation between MIF, AP-1 and MMP-9 concentrations and the Gensini score of coronary artery lesions (all P < 0.05). AP-1 was positively correlated with MMP-9 in CHD patients (P < 0.05). Plasma MIF, AP-1 and MMP-9 concentrations were positively correlated to the severity of coronary lesions in CHD patients. Higher MIF, AP-1 and MMP-9 concentrations in ACS patients than in SAP patients might suggest higher plaque instability in ACS patients.
    No preview · Article · Oct 2008 · Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases]
  • Gui-Hua Miao · Li-Xia Yang · Feng Qi · Xian-Mei Wang · Yan-Kun Shi · Ming-Qiu Li
    [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the relation between activator protein-1 (AP-1) and coronary atherosclerotic changes and the potential role of AP-1 in the stabilization of atherosclerotic plaques in patients with coronary heart disease (CHD). 142 patients were included in this study and divided into CHD group (107) and control group (35) according to coronary angiography (CAG). The CHD group was further divided into a stable angina pectoris (SAP) group (32) and an acute coronary syndrome (ACS) group (75) according to the clinical manifestations. In addition, the CHD group was divided into A type group, B type group and C type group according to the standard of ACC/AHA coronary change in 1988. Meanwhile, the CHD group was further divided into light stenosis group, moderate stenosis group and severe stenosis group according to the degree of coronary lesion. The lysate of cells was obtained through lysis of the leucocytes from peripheral blood with cell lysis buffer. The amount of Phospho-c-Jun in lysate was measured with enzyme-linked immunosorbent assay (ELISA). The results were demonstrated with absorbance, which reflects the amount of AP-1. The main coronary changes in the SAP group were A type (68.7%) and the changes were mainly of light degree (53.1%); the main coronary changes in the ACS group were B type (52.0%) or C type (37.3%) and the changes were mainly of heavy degree (66.7%). The absorbance of Phospho-c-Jun in CHD group was significantly higher than that in the control subjects (1.43 +/- 0.33 vs 0.71 +/- 0.13, P < 0.001). The absorbance of Phospho-c-Jun in the ACS group was significantly higher than that in the SAP group (1.56 +/- 0.28 vs 1.14 +/- 0.25, P < 0.001). The absorbance of Phospho-c-Jun increased gradually from A type group to C type group (1.18 +/- 0.27 vs 1.42 +/- 0.26 vs 1.71 +/- 0.27, P < 0.001) and from light stenosis group to severe stenosis group (1.09 +/- 0.20 vs 1.37 +/- 0. 26 vs 1.60 +/- 0.29, P < 0.001). There is a significant relationship between AP-1 and coronary atherosclerotic changes. AP-1 may be a factor that can predict coronary arteriosclerotic progression and stability of the plaque.
    No preview · Article · Aug 2008 · Zhonghua nei ke za zhi [Chinese journal of internal medicine]
  • [Show abstract] [Hide abstract]
    ABSTRACT: To observe the relationship between murine double minute 2 (mdm2) expression and AngII and ceramide induced human umbilical endothelial cells apoptosis. Human umbilical endothelial cells (ECs) were cultured in vitro and treated with angiotensin II alone or in combination with losartan (an inhibitor of AT1), PD123319 (an inhibitor of AT2) and FB1 (an inhibitor of ceramidase) respectively. ECs were also treated with different doses of C2-ceramide. The apoptosis of ECs was detected with Tunel, the mdm2 mRNA and protein expressions were measured with reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. PD123319 and FB1 but not losartan inhibited AngII induced ECs apoptosis and down-regulated the AngII induced increased mdm2 expressions. C2-ceramide also induces ECs apoptosis and down-regulated mdm2 expressions at protein and mRNA levels in a dose-dependent manner. AngII binding with AT2 induces ECs apoptosis via ceramide. AngII and ceramide induce EC apoptosis by inhibiting mdm2.
    No preview · Article · Nov 2007 · Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases]
  • Rui-Wei Guo · Li-Xia Yang · Mao-Quan Li · Bei Liu · Xian-Mei Wang
    [Show abstract] [Hide abstract]
    ABSTRACT: Angiotensin II (Ang II) is the main active peptide of the renin-angiotensin system (RAS), producing a number of inflammatory mediators that lead to endothelial dysfunction and the progression of atherosclerosis. Ang II-induced NF-kappaB nuclear translocation plays a pivotal role in this response. This study examines the NF-kappaB activation mechanism elicited by Ang II in human umbilical vein endothelial cells (HUVEC). Electrophoretic mobility shift assays and Western blotting revealed that Ang II, signaling via AT(1), produces a time-dependent increase in NF-kappaB DNA binding and IkappaBalpha degradation. These results also demonstrate that Ang II leads to MAPK phosphorylation and p38MAPK pathway-induced NF-kappaB activation. Furthermore, AT(1) is required for p38MAPK phosphorylation induced by Ang II. This study provides evidence that Ang II elicits NF-kappaB activation via the p38MAPK pathway in HUVEC.
    No preview · Article · Jan 2007 · Peptides
  • [Show abstract] [Hide abstract]
    ABSTRACT: The cytokine tumor necrosis factor (TNF) alpha has been causally linked to left ventricular (LV) remodeling, but the molecular basis for this effect is unknown. It is essential to study the changes of plasma levels of TNF alpha and matrix metalloproteinase-2,3,9 (MMP-2,3,9) expressions in myocardium during congestive heart failure (CHF). Plasma levels of TNF alpha were measured with enzyme-linked immunoassay in CHF patients of various degrees and in healthy controls. Using Western blotting assay, we detected the protein expressions of MMP-2,3,9 on myocardial tissue in CHF patients and in healthy controls. Cardiac function parameters were measured with echocardiographic studies. Plasma levels of TNF alpha increased significantly in patients with CHF (P < 0.05 or < 0.01). The protein expressions of MMP-2,3,9 were significantly higher in patients with CHF than in controls (P < 0.05 or < 0.01). The higher the degree of CHF, the greater the numbers of expressions. No changes of MMP-2 could be found between the controls and CHF patients of NYHA II. There was a positive correlation between plasma levels of TNF alpha and the protein expressions of MMP-2,3,9 (P < 0.01 or < 0.001). It is suggested that alterations of TNF alpha may stimulate the expressions of MMPs, contribute to myocardial remodeling and lead to the development and progression of congestive heart failure. These changes may induce a direct effect on the progression and deterioration of heart failure.
    No preview · Article · Nov 2004 · Zhonghua nei ke za zhi [Chinese journal of internal medicine]
  • [Show abstract] [Hide abstract]
    ABSTRACT: Stroke is a complex disorder caused by a combination of genetic and environmental factors. Epidemiological studies have provided evidence of genetic influence on the development of human stroke. However, genetic changes which contribute to the development of stroke are not well known. This study was designed to gain a deep insight into that aspect. Using cold-stimuli plus high-salt intake as environmental risk factors, the authors established a hypertension model in rats, which produced a complication of stroke. Then, they used the suppression subtractive hybridization(SSH) technique to identify the differential genes that specifically expressed in total cerebrum tissue of the rats in stroke group. A comparison was made between two populations, namely the control group and stroke group. By the use of SSH approach, a total of 576 clones were generated in this study from two subtractive libraries, among them 456 clones were usable and were analyzed. Genes for metabolism transcripts in stroke group were shown to be up-regulated (P<0.01). Mitochondrial transcripts were observed in a high rate of 26.5%. The findings suggested that mitochondrial genes should induce an increased sensitivity to stroke through the changes of gene expressions. Mitochondrial genes probably play important roles in the causes and effects of stroke.
    No preview · Article · Apr 2004 · Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics