Yong Jiang

Publications (3)13.45 Total impact

• Source

  Available from: PubMed Central

  Article: Disabled-2 (Dab2) inhibits Wnt/β-catenin signalling by binding LRP6 and promoting its internalization through clathrin.

  Yong Jiang, Xi He, Philip H Howe
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  ABSTRACT: Canonical Wnt signalling requires caveolin-dependent internalization of low-density lipoprotein receptor-related protein 6 (LRP6). Here we report that the tumour suppressor and endocytic adaptor disabled-2 (Dab2), previously described as an inhibitor of Wnt/β-catenin signalling, selectively recruits LRP6 to the clathrin-dependent endocytic route, thereby sequestering it from caveolin-mediated endocytosis. Wnt stimulation induces the casein kinase 2 (CK2)-dependent phosphorylation of LRP6 at S1579, promoting its binding to Dab2 and internalization with clathrin. LRP6 receptor mutant (S1579A), deficient in CK2-mediated phosphorylation and Dab2 binding, fails to associate with clathrin, and thus escapes the inhibitory effects of Dab2 on Wnt/β-catenin signalling. Our data suggest that the S1579 site of LRP6 is a negative regulatory point during LRP6-mediated dorsoventral patterning in zebrafish and in allograft mouse tumour models. We conclude that the tumour suppressor functions of Dab2 involve modulation of canonical Wnt signalling by regulating the endocytic fate of the LRP6 receptor.
  The EMBO Journal 04/2012; 31(10):2336-49. · 9.20 Impact Factor
• Article: A systematic review of modern metal-on-metal total hip resurfacing vs standard total hip arthroplasty in active young patients.

  Yong Jiang, Kaifang Zhang, Jun Die, Zhibing Shi, Haien Zhao, Kunzheng Wang
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  ABSTRACT: This systematic review compared 2 treatments for hip disease in active young patients: modern metal-on-metal total hip resurfacing and standard total hip arthroplasty. We conducted a literature search to identify relevant randomized and clinical controlled trials and included 968 patients from 4 trials in our analysis. Our results indicated increased rates of revision, femoral neck fractures, and component loosening among patients who received modern metal-on-metal hip resurfacing. No significant differences in the rates of mortality, dislocation, or deep hip joint infection were found between treatment groups. Hip function scores were similar between the 2 groups, but the resurfacing group showed higher activity levels. These results have provided insufficient evidence to determine whether modern metal-on-metal total hip resurfacing offers clinical advantages over standard total hip arthroplasty.
  The Journal of arthroplasty 04/2011; 26(3):419-26. · 1.79 Impact Factor
• Article: Rosuvastatin preconditioning provides neuroprotection against spinal cord ischemia in rats through modulating nitric oxide synthase expressions.

  Jun Die, Kunzheng Wang, Lihong Fan, Yong Jiang, Zhibing Shi
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  ABSTRACT: The study was aimed to investigate the protective effects of rosuvastatin on spinal cord ischemia in rats and to determine the effects of this agent on the expressions of nitric oxide synthase (NOS). Spinal cord ischemia was induced in male Sprague-Dawley rats by occluding the descending thoracic aorta. Experimental groups (n=30 per group) were as follows: sham operation, control (receiving only normal saline), rosuvastatin (5 mg/kg/day for 10 days before occlusion), and rosuvastatin-mevalonate (5 mg/kg/day rosuvastatin and 5 mg/kg/day mevalonate for 10 days before occlusion). Neurological function was assessed at 6, 12, 24, 48, and 72 h after reperfusion. After 72 h reperfusion, spinal cords were harvested for 2,3,5,-triphenyltetrazolium chloride (TTC) staining, TUNEL staining, and nitric oxide (NO) assay. Immunohistochemistry, reverse transcription polymerase chain reaction and western blot were performed to determine the expressions of inducible, endothelial, and neuronal NOS (iNOS, eNOS, and nNOS) in rats with spinal cord ischemia. Spinal cord ischemia thus induced was marked by neurological dysfunction, spinal infarction, and neural cell apoptosis in animals. The results show that rosuvastatin significantly reduced the motor disturbance and the volume of infarctions and attenuated apoptotic neural cells death in the treated rats. Treatment with rosuvastatin remarkably decreased the NO level in spinal cord tissue. In addition, rosuvastatin inhibited iNOS mRNA and protein expression and increased eNOS mRNA and protein expression. However, rosuvastatin had no influence on nNOS mRNA and protein expression. Administrations of mevalonate completely reversed the changes caused by rosuvastatin. These results indicate that rosuvastatin can protect rat spinal cord against ischemia injury by modulation of NOS expressions.
  Brain research 07/2010; 1346:251-61. · 2.46 Impact Factor