Xiao Yang

Jishou University, So-li, Hunan, China

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Publications (222)774.65 Total impact

  • Clinical chemistry and laboratory medicine : CCLM / FESCC. 09/2014;
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    ABSTRACT: Monocyte chemoattractant protein-1 (MCP-1) is an important chemokine involved in the pathogenesis of spontaneous preterm birth (SPTB). We examined whether the MCP-1 G-2518A polymorphism is associated with the risk of SPTB in a Chinese population. The MCP-1 G-2518A polymorphism was genotyped in 569 preterm singleton neonates and in 673 term neonates using polymerase chain reaction-restriction fragment length polymorphism analysis. The distribution of the MCP-1 G-2518A genotype and the allele frequencies between the SPTB patients and the controls were not significantly different in the overall sample. However, we found that the AA genotype was associated with significantly increased susceptibility to very SPTB (<32 weeks) [odds ratio (OR) 2.07; 95 % confidence interval (CI), 1.27-3.36; P = 0.005) and extremely SPTB (<28 weeks) (OR 2.74; 95 % CI, 1.10-6.72; P = 0.014) compared with -2518G-positive genotypes (GG + GA genotypes). When extremely preterm neonates and very preterm neonates were combined, the AA genotype was also significantly associated with increased susceptibility to SPTB (OR 2.23; 95 % CI, 1.40-3.54; P < 0.001). The MCP-1 G-2518A polymorphism was not associated with increased susceptibility to SPTB in patients with premature rupture of the membranes (PROM) or in those without PROM. Our findings suggest that the MCP-1 G-2518A polymorphism may plays a role in mediating the susceptibility to SPTB in the Chinese population. Knowledge of genetic factors contributing to the pathogenesis of SPTB may have implications for screening and treatment of this disorder.
    Molecular genetics and genomics : MGG. 09/2014;
  • Peritoneal dialysis international: journal of the International Society for Peritoneal Dialysis 09/2014; · 2.21 Impact Factor
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    Cell research. 08/2014;
  • International journal of cardiology. 08/2014;
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    ABSTRACT: Cystatin play an important role in parasite immune evasion. It is involved in many immune responses processes regulations such as inhibiting antigen presentation, modifying cytokines production and macrophage polarization. In recent years, more and more cystatins were used in treating some inflammatory diseases such as asthma and inflammation bowel diseases; however, cystatins from Schistosoma japonicum were rarely studied. In the present study, we have cloned a cystatin from the adult stage of Schistosoma japonicum, named as SjCystatin, and its sequence shares conserved domains with other type II family cystatins. It was further verified by enzyme inhibition assays. SjCystatin retained its inhibitory activity under a wide range of pH values and temperatures, can maintain its inhibitory activity at pH 6.5-7.5 and 37 °C, respectively. Then, we investigated the effects of SjCystatin on the lipopolysaccharide (LPS)-induced activated RAW264.7. Results showed that SjCystatin inhibit LPS-induced nitric oxide production in a dose-dependent manner. LPS-induced TNF-α and IL-6 production began to be inhibited at least 6 h after SjCystatin stimulation. SjCystatin significantly increased IL-10 production at 6 h after stimulation and its effect on IL-10 production diminished quickly. These results imply that SjCystatin can induce M2 macrophage polarization and can be expected to serve as a potential drug source for the medication of inflammatory disorders like other cystatins.
    Parasitology research. 08/2014;
  • Yu Lan, Wenyan He, Bing Liu, Xiao Yang
    Experimental hematology. 08/2014; 42(8S):S44.
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    ABSTRACT: Retinoic acid-inducible gene I (RIG-I) is an intracellular RNA virus sensor that induces type I interferon-mediated host protective innate immunity against viral infection. Although cylindromatosis (CYLD) has been shown to negatively regulate innate antiviral response by removing K-63-linked polyubiquitin from RIG-I, the regulation of its expression and the underlying regulatory mechanisms are still incompletely understood. Here we show that RIG-I activity is regulated by miR-526a-mediated inhibition of CYLD expression. We found that viral infection specifically upregulates miR-526a expression in macrophages via IRF-dependent mechanisms. In turn, miR-526a positively regulates virus-triggered type I Interferon (IFN-I) production, thus suppressing viral replication, the underlying mechanism of which is the enhancement of RIG-I K63-linked ubiquitination by miR-526a via suppressing the expression of CYLD. Remarkably, viral-induced miR-526a upregulation and CYLD downregulation are blocked by enterovirus 71 (EV71) 3C protein, while ectopic miR-526a expression inhibits the replication of EV71 virus. The collective results of this study suggest a novel mechanism of the regulation of RIG-I activity during RNA virus infection by miR-526a and propose a novel mechanism for the evasion of innate immune response controlled by EV71.
    Journal of virology. 07/2014;
  • Xiaoguang Fan, LEI Ming, XIAO Yang
    WCS2014; 07/2014
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    ABSTRACT: We have shown recently that endothelial Grb-2-associated binder 1 (Gab1), an intracellular scaffolding adaptor, has a protective effect against limb ischemia via mediating angiogenic signaling pathways. However, the role of Gab1 in cardiac ischemia/reperfusion (I/R) injury remains unknown. In this study, we show that Gab1 is required for cardioprotection against I/R injury. I/R injury led to remarkable phosphorylation of Gab1 in cardiomyocytes. Compared with controls, the mice with cardiomyocyte-specific deletion of Gab1 gene (CGKO mice) exhibited an increase in infarct size and a decrease in cardiac function after I/R injury. Consistently, in hearts of CGKO mice subjected to I/R, the activation of caspase 3 and myocardial apoptosis was markedly enhanced whereas the activation of protein kinase B (Akt) and mitogen-activated protein kinase (MAPK), which are critical for cardiomyocyte survival, was attenuated. Oxidative stress is regarded as a major contributor to myocardial I/R injury. To examine the role of Gab1 in oxidative stress directly, isolated adult cardiomyocytes were subject to oxidant hydrogen peroxide and the cardioprotective effects of Gab1 were confirmed. Furthermore, we found that the phosphorylation of Gab1 and Gab1-mediated activation of Akt and MAPK by oxidative stress was suppressed by ErbB receptor and Src kinase inhibitors, accompanied by an increase in apoptotic cell death. In conclusion, our results suggest that Gab1 is essential for cardioprotection against I/R oxidative injury via mediating survival signaling.
    Basic research in cardiology. 07/2014; 109(4):420.
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    ABSTRACT: The study was to investigate the prevalence and associated factors of erectile dysfunction (ED) in peritoneal dialysis (PD) patients.
    International Urology and Nephrology 06/2014; · 1.33 Impact Factor
  • Xueqing Yu, Xiao Yang, Naya Huang
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    ABSTRACT: Managing a rapidly growing peritoneal dialysis program with more than 1000 patients involves multiple challenges, labor constraints, logistics, and excessive geographic distance. This paper describes how Sun Yat-sen University, Guangzhou, China, manages those issues, while simultaneously improving quality of the care and, subsequently, clinical outcomes.
    Peritoneal dialysis international: journal of the International Society for Peritoneal Dialysis 06/2014; 34(Supplement 2):S31-S34. · 2.21 Impact Factor
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    ABSTRACT: In mouse, continuous growth of the postnatal incisor is coordinated by two populations of multipotent progenitor cells, the dental papilla mesenchymal cells and dental epithelial stem cells, residing at the proximal end of the incisor, yet the molecular mechanism underlying the cooperation between mesenchymal and epithelial cells is largely unknown. Here, TGF-β type II receptor (Tgfbr2) was specifically deleted within the postnatal dental papilla mesenchyme. The Tgfbr2-deficient mice displayed malformed incisors with wavy mineralized structures at the labial side as a result of increased differentiation of dental epithelial stem cells. We found that mesenchymal Tgfbr2 disruption led to upregulated expression of Wnt5a and downregulated expression of Fgf3/10 in the mesenchyme, both of which synergistically enhanced Lrp5/6-β-catenin signaling in the cervical loop epithelium. In accord with these findings, mesenchyme-specific depletion of the Wnt transporter gene Wls abolished the aberrant mineralized structures caused by Tgfbr2 deletion. Thus, mesenchymal TGF-β signaling provides a unifying mechanism for the homeostasis of dental epithelial stem cells via a Wnt signaling mediated mesenchymal–epithelial cell interaction. Stem Cells 2014
    Stem Cells 06/2014; · 7.70 Impact Factor
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    ABSTRACT: Aristolochic acid I (AAI) can induce renal tubular epithelial cells (RTECs) autophagy, which thereby extenuates apoptosis in vitro. In this study, we aimed to determine whether the in vitro data also apply to the AAI-induced pathologic condition in vivo. BALB/c mice were treated with AAI, autophagy inhibitors [3-methyladenine (3MA) or chloroquine diphosphate salt (CQ)], and AAI plus the inhibitors for consecutive 5 days, respectively. Mice were euthanized on day 3 and 5. AAI induced RTECs autophagy was confirmed by electron microscopy and western blot. The results showed induction of apoptotic RTECs and up-regulation of mitochondrial and endoplasmic reticulum stress-related proteins in AAI-treated mice at both of the two time points. There were more apoptotic RTECs in AAI + inhibitor groups, which might be due to increased mitochondrial stress-related proteins (cytochrome C and apoptotic protease activating factor 1, APAF-1). On day 5, severe tubulointerstitial injuries induced by AAI led to a significant decline in kidney function. There were numerous autolysosomes in dying RTECs of the AAI group. Autophagy inhibitors increased AAI-induced RTECs mitochondrial apoptosis by increasing mitochondrial stress-related proteins, but they partially mitigated the AAI-induced severe renal tubulointerstitial injury. These results confirmed that AAI could induce autophagy in RTECs, which prevented apoptosis via mitochondrial pathway in vivo. However, continuous stimulation with AAI induced excess autophagy, which ultimately resulted in AAI-induced cell death. It suggested that apoptosis wasn't the main culprit in acute aristolochic acid nephropathy mice model.
    APOPTOSIS 05/2014; · 3.95 Impact Factor
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    ABSTRACT: Colonic immune homeostasis is essential for normal gastrointestinal tract functioning. In this study, we report that specific gene targeting of phosphatase and tensin homolog (PTEN) in smooth muscle cells caused age-related colonic lymphoid hyperplasia followed by global immune activation in mice. Beginning at 5 weeks of age, these mutant mice displayed massive neutrophil infiltration in the colonic lamina propria. The gene expression levels of pro-inflammatory cytokines and chemokines, including those code for monocyte chemotactic protein-1 (Mcp-1), stromal cell-derived factor 1α (Sdf-1α), and chemokine (C-C motif) ligand 28 (Ccl-28), were upregulated in the colon. Accordingly, permeability and proliferation of the colonic epithelium was compromised. These abnormalities were alleviated to a great extent when the mutants were crossed with Akt1-null mice, indicating that the pathogenesis was mediated by Akt1 signaling. Our results suggest that in smooth muscle cells, PTEN is crucial for maintaining colonic immune homeostasis.
    The international journal of biochemistry & cell biology 05/2014; · 4.89 Impact Factor
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    ABSTRACT: Natural killer (NK) cell activation is well orchestrated by a wide array of NK cell receptor repertoire. TIGIT receptor was recently defined as an inhibitory receptor that is expressed on NK cells and T cells. TIGIT receptor/PVR ligand engagement signaling inhibits cytotoxicity mediated by NK and CD8+ T cells. However, it is unclear how TIGIT/PVR signaling regulates cytokine secretion in NK cells. Here we show that TIGIT/PVR engagement suppresses interferon-γ(IFN-γ) production of NK cells. TIGIT transgenic NK cells generate less IFN-γ undergoing TIGIT/PVR ligation. Moreover, TIGIT knockout NK cells produce much more IFN-γ. TIGIT/PVR ligation signaling mediates suppression of IFN-γ production via NF-κB pathway. We identified a novel adaptor β-arrestin 2 that associates with phosphorylated TIGIT for further recruitment of SHIP1 (SH2-containing inositol phosphatase 1) through the ITT-like motif. Importantly, SHIP1, but not other phosphatases, impairs the TNF receptor associated factor 6 (TRAF6) autoubiquitination to abolish NF-κB activation, leading to suppression of IFN-γ production in NK cells.
    Journal of Biological Chemistry 05/2014; · 4.65 Impact Factor
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    ABSTRACT: In mouse mid-gestational embryos, definitive hematopoietic stem progenitor cells are derived directly from a very small proportion of the arterial endothelium. However, the physiological mechanisms restraining excessive endothelial-hematopoietic transition remain elusive. We show here that genetic deletion of Smad4 from the endothelium stage (using Tie2-Cre), but not from embryonic hematopoietic cells (using Vav-Cre), leads to a strikingly augmented emergence of intra-arterial hematopoietic clusters and an enhanced in vitro generation of hematopoietic progenitors, with no increase in the proliferation and survival of hematopoietic cluster cells. This finding indicates a temporally restricted negative effect of Smad4 on the endothelial to hematopoietic progenitor transition. Furthermore, the absence of endothelial Smad4 causes an increased expression of sub-aortic bone morphogenetic protein 4 and an activation of aortic ERK, thereby resulting in the excessive generation of blood cells. Collectively, our data for the first time identify a physiological suppressor that functions specifically during the transition of endothelial cells to hematopoietic progenitors and further suggest that endothelial Smad4 is a crucial modulator of the sub-aortic microenvironment that controls the hematopoietic fate of the aortic endothelium.
    Blood 02/2014; · 9.78 Impact Factor
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    ABSTRACT: In this paper, we present a novel surface imprinting technique for the preparation of molecularly imprinted polymers/multi-walled carbon nanotubes (MIPs/MWNTs) for extraction of emodin from kiwi fruit root. The MIPs/MWNTs were characterised by scanning electron microscopy (SEM) and Fourier transform-infrared spectroscopy (FT-IR). The properties involving adsorption dynamics, static adsorption, and selective recognition capacity were evaluated. The MIPs/MWNTs exhibited good site accessibility in which it only took 60min to achieve adsorption equilibrium and highly selective recognition for the template emodin. Furthermore, the performance of the MIPs/MWNTs as solid phase extraction (SPE) material was investigated in detail. The proposed MIPs/MWNTs-SPE procedure for emodin exhibited satisfactory recoveries ranging from 89.2% to 93.8% for real samples. It was used for the purification and enrichment of emodin from kiwi fruit root successfully.
    Food Chemistry 02/2014; 145C:687-693. · 3.33 Impact Factor
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    ABSTRACT: Impaired phosphatase activity contributes to the persistent activation of STAT3 in tumors. Given that STAT family members with various or even opposite functions are often phosphorylated or dephosphorylated by the same enzymes, the mechanism for STAT3-specific dephosphorylation in cells remains largely unknown. Here, we report that GdX (UBL4A) promotes STAT3 dephosphorylation via mediating the interaction between TC45 (the nuclear isoform of TC-PTP) and STAT3 specifically. GdX stabilizes the TC45-STAT3 complex to bestow upon STAT3 an efficient dephosphorylation by TC45. Inasmuch, GdX suppresses tumorigenesis and tumor development by reducing the level of phospho-STAT3 (p-STAT3), whereas deletion of GdX results in a high level of p-STAT3 and accelerated colorectal tumorigenesis induced by AOM/DSS. Thus, GdX converts TC45, a nonspecific phosphatase, into a STAT3-specific phosphatase by bridging an association between TC45 and STAT3.
    Molecular cell 02/2014; · 14.61 Impact Factor
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    ABSTRACT: Escherichia coli peritonitis is one frequent, serious complication of peritoneal dialysis (PD). The extended-spectrum β-lactamase (ESBL)-producing E. coli peritonitis is associated with poorer prognosis and its incidence has been on continuous increase during the last decades. However, the clinical course and outcomes of E. coli peritonitis remain largely unclear. All of the E. coli peritonitis episodes occurred in our dialysis unit from 2006 to 2011 was reviewed. The polymicrobial episodes were excluded. Totally, ninety episodes of monomicrobial E. coli peritonitis occurred in 68 individuals, corresponding to a rate of 0.027 episodes per patient-year. E. coli was the leading cause (59.2%) of monomicrobial gram-negative peritonitis. ESBL-producing strains accounted for 35.5% of E. coli peritonitis. The complete cure rate and treatment failure rate of E. coli peritonitis were 77.8% and 10.0% respectively. Patients with preceding peritonitis had a higher risk of ESBL production as compared to those without peritonitis history [odds ratio (OR): 5.286; 95% confidence interval (CI): 2.018 - 13.843; p = 0.001]. The risk of treatment failure was significantly increased when patient had a baseline score of Charlson Comorbidity Index (CCI) above 3 (OR: 6.155; 95% CI: 1.198 - 31.612; p = 0.03), or had diabetes mellitus (OR: 8.457; 95% CI: 1.838 - 38.91; p = 0.006), or hypoalbuminemia (≤ 30g/l) on admission (OR: 13.714; 95% CI: 1.602 - 117.428; p = 0.01). Prolonging treatment course from 2 to 3 weeks or more reduced the risk of relapse and repeat significantly (p < 0.05). E. coli peritonitis remains a common complication of PD. The clinical outcomes of E. coli peritonitis is relatively favorable despite of the high ESBL rate. A history of peritonitis is associated with increased risk for ESBL development. The severity of baseline comorbidities, the presence of diabetes mellitus and hypoalbuminemia on admission is associated with poor outcomes.
    Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis. 02/2014;

Publication Stats

3k Citations
774.65 Total Impact Points

Institutions

  • 2010–2014
    • Jishou University
      So-li, Hunan, China
    • Lanzhou University
      • School of Life Science
      Lanzhou, Gansu Sheng, China
  • 2004–2014
    • Sun Yat-Sen University
      Shengcheng, Guangdong, China
  • 2002–2014
    • Sun Yat-Sen University of Medical Sciences
      • Department of Nephrology
      中山, Guangdong, China
  • 2001–2014
    • Fuerkang Beijing Institute of Biotechnology
      Peping, Beijing, China
  • 2013
    • HudsonAlpha Institute for Biotechnology
      Huntsville, Alabama, United States
  • 2009–2013
    • Chinese PLA General Hospital (301 Hospital)
      Peping, Beijing, China
    • 307 Hospital of the Chinese People's Liberation Army
      Peping, Beijing, China
  • 2012
    • Xinqiao Hospital
      Ch’ung-ch’ing-shih, Chongqing Shi, China
    • Chinese Academy of Sciences
      • Graduate School
      Peping, Beijing, China
  • 2011
    • Shanghai Jiao Tong University
      Shanghai, Shanghai Shi, China
  • 2008–2011
    • Northeast Institute of Geography and Agroecology
      • Institute of Biophysics
      Beijing, Beijing Shi, China
  • 2000–2010
    • Academy of Military Medical Sciences
      T’ien-ching-shih, Tianjin Shi, China
  • 2005–2009
    • Government of the People's Republic of China
      Peping, Beijing, China
    • Beijing Institute of Microbiology and Epidemiology
      Peping, Beijing, China
    • Guangzhou First People's Hospital
      Shengcheng, Guangdong, China
    • Institute of Genetics & Hospital for Genetic Diseases
      Bhaganagar, Andhra Pradesh, India
  • 2007
    • Shanghai University
      • Department of Automation
      Shanghai, Shanghai Shi, China
  • 2006
    • Peking Union Medical College Hospital
      Peping, Beijing, China
  • 2003
    • Henan Provincial People’s Hospital
      Cheng, Henan Sheng, China
  • 1997–2002
    • National Institutes of Health
      • • Branch of Genetics of Development and Disease (GDDB)
      • • Laboratory of Metabolism
      Bethesda, MD, United States