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Articles by W Qin
Total Records ( 6 ) for W Qin
  B Huang , W Qin , B Zhao , Y Shi , C Yao , J Li , H Xiao and Y. Jin
 

MicroRNAs (miRNAs), which are a newly identified class of small single-stranded non-coding RNAs, regulate their target genes via post-transcriptional pathway. It has been proved that miRNAs play important roles in many biological processes. To better understand miRNA function on type 2 diabetes, we used an oligonucleotide microarray to monitor miRNA expression profiles of Goto–Kakizaki (GK) and Wistar rats' skeletal muscle. It was found that seven miRNAs were down-expressed and two miRNAs were over-expressed in the muscle of GK rats. Among them, miR-24 showed the most prominent change. p38 MAPK, which is a direct target of miR-24, also showed expression difference. All the data give a clue that miR-24 might be associated with diabetes through down-regulation of p38 MAPK.

  W Qin , B Zhao , Y Shi , C Yao , L Jin and Y. Jin
 

MicroRNAs (miRNAs) are a type of small non-coding RNAs that regulate cognate mRNA expressions at the post-transcriptional stage. Although several miRNAs are known to be involved in various biological processes, including developmental timing, patterning, embryogenesis, differentiation and organogenesis, growth control, and apoptosis, many target genes and the functions of most miRNAs are still unclear. Since there is only a partial complementarity between miRNAs and their targets in animal cells, it is difficult to identify the specific target genes for a given miRNA and elucidate its function. In this study, we confirmed that bone morphogenetic protein receptor II (BMPRII) is a direct target of miR-21, and also showed that the protein level of BMPRII correlates inversely with the amount of miR-21 in PC3 and Lncap cells. These findings suggest that miR-21 may have a potential role in regulating the malignancy and metastatic abilities of prostate cancer cells and in self-renewal of stem cells by regulating the expression of BMPRII.

  Y Xie , M Wu , R Song , J Ma , Y Shi , W Qin and Y. Jin
 

Regulatory T (Treg) cells are a subpopulation of T cells that not only prevent autoimmunity, but also control a wide range of T cell-dependent immune responses. Glucocorticoid treatment (dexamethasone, or Dex) has been reported to amplify IL-2-mediated selective in vivo expansion of Treg cells. We simultaneously administered Dex and IL-2 to the donor in a murine allogeneic lymphocyte transplantation model to expand functional suppressive CD4+CD25+FOXP3+ T cells in the graft and to raise the regulatory T cell/effector T cell (Treg/Teff) ratio to prevent graft-versus-host disease (GVHD). After combined treatment of the donor with Dex (5 mg/kg/day) and IL-2 (300,000 IU/mouse/day) for 3 days, grafts were subjected to flow cytometric analysis, and transplantation was carried out from male C57BL/6 mice to female BALB/c mice aged 8–12 weeks. Results showed that short-term simultaneous administration of Dex and IL-2 markedly expanded functional suppressive CD4+CD25+FOXP3+ T cells in the murine spleen. In this murine allogeneic transplantation model, the grafts from donors with Dex and IL-2 pre-treatment led to a longer survival time for the recipients than for the control group (median survival time > 60 day vs. 12 day, P = 0.0002). The ratio of Treg/Teff also increased remarkably (0.43 ± 0.15 vs. 0.14 ± 0.01, P = 0.01). This study demonstrated that co-stimulation with Dex and IL-2 selectively expanded functional CD4+CD25+FOXP3+ T cells in vivo, and that grafts from donors pre-treated with Dex and IL-2 led to longer survival time and greater suppression of GVHD after allogeneic transplantation. Thus, GVHD can be suppressed by the specific expansion of regulatory T cells with Dex and IL-2 in graft donors.

  L Wang , C Yu , H Chen , W Qin , Y He , F Fan , Y Zhang , M Wang , K Li , Y Zang , T. S Woodward and C. Zhu
 

Numerous studies argue that cortical reorganization may contribute to the restoration of motor function following stroke. However, the evolution of changes during the post-stroke reorganization has been little studied. This study sought to identify dynamic changes in the functional organization, particularly topological characteristics, of the motor execution network during the stroke recovery process. Ten patients (nine male and one female) with subcortical infarctions were assessed by neurological examination and scanned with resting-state functional magnetic resonance imaging across five consecutive time points in a single year. The motor execution network of each subject was constructed using a functional connectivity matrix between 21 brain regions and subsequently analysed using graph theoretical approaches. Dynamic changes in topological configuration of the network during the process of recovery were evaluated by a mixed model. We found that the motor execution network gradually shifted towards a random mode during the recovery process, which suggests that a less optimized reorganization is involved in regaining function in the affected limbs. Significantly increased regional centralities within the network were observed in the ipsilesional primary motor area and contralesional cerebellum, whereas the ipsilesional cerebellum showed decreased regional centrality. Functional connectivity to these brain regions demonstrated consistent alterations over time. Notably, these measures correlated with different clinical variables, which provided support that the findings may reflect the adaptive reorganization of the motor execution network in stroke patients. In conclusion, the study expands our understanding of the spectrum of changes occurring in the brain after stroke and provides a new avenue for investigating lesion-induced network plasticity.

  B. M Zeigler , J Vajdos , W Qin , L Loverro and K. Niss
  Brandon M. Zeigler, Janis Vajdos, Wenning Qin, Linda Loverro, and Knut Niss

In mammals, the production of red blood cells is tightly regulated by the growth factor erythropoietin (EPO). Mice lacking a functional Epo gene are embryonic lethal, and studying erythropoiesis in EPO-deficient adult animals has therefore been limited. In order to obtain a preclinical model for an EPO-deficient anemia, we developed a mouse in which Epo can be silenced by Cre recombinase. After induction of Cre activity, EpoKO/flox mice experience a significant reduction of serum EPO levels and consequently develop a chronic, normocytic and normochromic anemia. Furthermore, compared with wild-type mice, Epo expression in EpoKO/flox mice is dramatically reduced in the kidney, and expression of a well-known target gene of EPO signaling, Bcl2l1, is reduced in the bone marrow. These observations are similar to the clinical display of anemia in patients with chronic kidney disease. In addition, during stress-induced erythropoiesis these mice display the same recovery rate as their heterozygous counterparts. Taken together, these results demonstrate that this model can serve as a valuable preclinical model for the anemia of EPO deficiency, as well as a tool for the study of stress-induced erythropoiesis during limiting conditions of EPO.

  N Gao , J Le Lay , W Qin , N Doliba , J Schug , A. J Fox , O Smirnova , F. M Matschinsky and K. H. Kaestner
 

Foxa1 and Foxa2 play both redundant and distinct roles in early pancreas development. We demonstrate here that inducible ablation of both transcription factors in mature mouse β-cells leads to impaired glucose homeostasis and insulin secretion. The defects in both glucose-stimulated insulin secretion and intracellular calcium oscillation are more pronounced than those in β-cells lacking only Foxa2. Unexpectedly, in contrast to the severe reduction of β-cell-enriched factors contributing to metabolic and secretory pathways, expression of a large number of genes that are involved in neural differentiation and function is significantly elevated. We further demonstrate that expression of carbohydrate response element-binding protein (ChREBP or Mlxipl), an important transcriptional regulator of carbohydrate metabolism, is significantly affected in compound Foxa1/a2 mutant β-cells. ChREBP expression is directly controlled by Foxa1 and Foxa2 in both the fetal endocrine pancreas as well as mature islets. These data demonstrate that Foxa1 and Foxa2 play crucial roles in the development and maintenance of β-cell-specific secretory and metabolic pathways.

 
 
 
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