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Articles by W Xing
Total Records ( 3 ) for W Xing
  J Kim , W Xing , J Wergedal , J. Y Chan and S. Mohan
 

Previous in vitro studies found that nuclear factor erythroid-derived 2-like 1 (NFE2L1) was involved in mediating ascorbic acid-induced osterix expression and osteoblast differentiation via binding to the antioxidant response element of the osterix promoter. To test the role of NFE2L1 in regulating bone formation in vivo, we disrupted NFE2L1 specifically in osteoblasts. Mice expressing Cre under the control of Col12 promoter were crossed with NFE2L1 loxP mice to generate Cre+ knockout (KO) and Cre– wild-type (WT) mice. Skeletal measurements by DEXA revealed 8–10% and 9–11% reduction in total body BMC and bone area in the KO mice from 3 to 8 wk of age. Peripheral quantitative computed tomography analyses found both periosteal and endosteal circumferences were reduced by 6% at the middiaphysis of the femurs from 8 wk old KO mice. Histomorphometric analyses revealed reduced bone formation was a cause for reduced bone size in the KO mice. Microcomputed tomography analysis of the metaphysis of the femur revealed that trabecular bone volume/total volume, and trabecular numbers were decreased by 30 and 53% in the NFE2L1 KO mice. Expression of osterix was decreased by 57% in the bones of NFE2L1 KO mice. In vitro nodule assay demonstrated that mineralized nodule area was reduced by 68% in the cultures of bone marrow stromal cells from NFE2L1 KO mice. Treatment of primary osteoblasts with ascorbic acid increased osterix expression by fourfold, whereas loss of NFE2L1 in osteoblasts diminished ascorbic acid stimulation of osterix expression by 50%. Our data provide the first in vivo experimental evidence that NFE2L1 produced by osteoblasts is involved in regulating osterix expression, osteoblast differentiation, and bone formation.

  X Shen , G. b Hu , S. j Jiang , F. r He , W Xing , L Li , J Yang , H. f Zhu , P Lei and G. x. Shen
 

Transferrin receptor (TfR) has been explored as a target for antibody-based therapy of cancer. In the previous study, we reported a murine anti-TfR monoclonal antibody (mAb) 7579 had good anti-tumor activities in vitro. In an attempt to reduce its immunogenicity and enhance its ability to recruit immune effector mechanism in vivo, we herein developed its chimera in the baculovirus/insect cell expression system based on the mating-assisted genetically integrated cloning (MAGIC) strategy. The chimeric light and heavy chains, containing human IgG1 constant regions, were correctly processed and assembled in insect cells, and then secreted into the mediums as heterodimeric H2L2 immunoglobulins. Furthermore, analyses of antigen-binding assay and competitive binding assay indicated that the chimeric antibody possessed specificity and affinity similar to that of its parental murine antibody. Results of the antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) assay verified that the chimeric antibody could efficiently mediate ADCC and CDC against TfR-overexpressing tumor cells. These results suggested that this baculovirus-expressed chimeric anti-TfR IgG1 might have the potential to be used for cancer immunotherapy. Meanwhile, the MAGIC strategy, facilitating the rapid generation of chimeric mAbs, could be one of the efficient strategies for antibody engineering.

  S Paruchuri , H Tashimo , C Feng , A Maekawa , W Xing , Y Jiang , Y Kanaoka , P Conley and J. A. Boyce
 

Of the potent lipid inflammatory mediators comprising the cysteinyl leukotrienes (LTs; LTC4, LTD4, and LTE4), only LTE4 is stable and abundant in vivo. Although LTE4 shows negligible activity at the type 1 and 2 receptors for cys-LTs (CysLT1R and CysLT2R), it is a powerful inducer of mucosal eosinophilia and airway hyperresponsiveness in humans with asthma. We show that the adenosine diphosphate (ADP)–reactive purinergic (P2Y12) receptor is required for LTE4-mediated pulmonary inflammation. P2Y12 receptor expression permits LTE4 -induced activation of extracellular signal-regulated kinase in Chinese hamster ovary cells and permits chemokine and prostaglandin D2 production by LAD2 cells, a human mast cell line. P2Y12 receptor expression by LAD2 cells is required for competition between radiolabeled ADP and unlabeled LTE4 but not for direct binding of LTE4, suggesting that P2Y12 complexes with another receptor to recognize LTE4. Administration of LTE4 to the airways of sensitized mice potentiates eosinophilia, goblet cell metaplasia, and expression of interleukin-13 in response to low-dose aerosolized allergen. These responses persist in mice lacking both CysLT1R and CysLT2R but not in mice lacking P2Y12 receptors. The effects of LTE4 on P2Y12 in the airway were abrogated by platelet depletion. Thus, the P2Y12 receptor is required for proinflammatory actions of the stable abundant mediator LTE4 and is a novel potential therapeutic target for asthma.

 
 
 
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