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Articles by G. Chen
Total Records ( 6 ) for G. Chen
  X Feng , H Huang , Y Yang , O Frohlich , J. D Klein , J. M Sands and G. Chen
 

The cell plasma membrane contains specialized microdomains called lipid rafts which contain high amounts of sphingolipids and cholesterol. Lipid rafts are involved in a number of membrane protein functions. The urea transporter UT-A1, located in the kidney inner medullary collecting duct (IMCD), is important for urine concentrating ability. In this study, we investigated the possible role of lipid rafts in UT-A1 membrane regulation. Using sucrose gradient cell fractionation, we demonstrated that UT-A1 is concentrated in the caveolae-rich fraction both in stably expressing UT-A1 HEK293 cells and in freshly isolated kidney IMCD suspensions. In these gradients, UT-A1 at the cell plasma membrane is codistributed with caveolin-1, a major component of caveolae. The colocalization of UT-A1 in lipid rafts/caveolae was further confirmed in isolated caveolae from UT-A1-HEK293 cells. The direct association of UT-A1 and caveolin-1 was identified by immunoprecipitation and GST pull-down assay. Examination of internalized UT-A1 in pEGFP-UT-A1 transfected HEK293 cells fluorescent overlap with labeled cholera toxin subunit B, a marker of the caveolae-mediated endocytosis pathway. Disruption of lipid rafts by methyl-β-cyclodextrin or knocking down caveolin-1 by small-interference RNA resulted in UT-A1 cell membrane accumulation. Functionally, overexpression of caveolin-1 in oocytes decreased UT-A1 urea transport activity and UT-A1 cell surface expression. Our results indicate that lipid rafts/caveolae participate in UT-A1 membrane regulation and this effect is mediated via a direct interaction of caveolin-1 with UT-A1.

  Y. Lin , Y. Xu , G. Chen , B. Huang , J. Yao , Z. Chen , L. Yao , F. Lin , Y. Qiao , Z. Chen , S. Zhu , H. Huang and J. Wen
  Objective  It has been suggested that serum γ-glutamyltransferase is independently associated with cardiovascular mortality and atherosclerosis. The present study is to investigate the relationship between serum γ-glutamyltransferase and potential associated damage in an adult She Chinese population.

Method  A multistage, stratified, cluster, random sampling method was used to select an ethnically representative group of individuals aged 20-80 years in the general population. Brachial-ankle pulse-wave velocity was used to assess arterial stiffness in the general population and the Toronto Clinical Neuropathy Scoring System was used to detect diabetic peripheral polyneuropathy among populations with diabetes.

Results  A total of 5385 subjects were entered into the analysis. Serum γ-glutamyltransferase levels were classified into four groups using the 25th, 50th and 75th percentiles as cut points (males: < 20, 20-29, 29-52 and > 52 U/l; females: < 13, 13-18, 18-25 and > 25 U/l). As compared with the first quartile, the relative risks of arterial stiffness were 1.418, 1.667 and 2.394 in the other three categories, respectively (test for trend P < 0.05). After adjustment in five models, serum γ-glutamyltransferase was still a risk factor of arterial stiffness. We found inverted U-shape curves in both genders and the third quartile (male: 29 52 U/l; female: 18-25 U/l) had the highest odds ratios of 1.640 and 1.529, respectively.

Conclusions  We demonstrated that high serum γ-glutamyltransferase concentrations were directly associated with the increased risk of arterial stiffness, in general, and with peripheral polyneuropathy in subjects with diabetes in an ethnic She Chinese population. Alcohol use, gender, BMI and blood pressure were related to serum γ-glutamyltransferase and were involved in the relationship between serum γ-glutamyltransferase and brachial-ankle pulse-wave velocity.

  H.K. Chandru and G. Chen
  Nitric oxide is known to regulate gene expression by modulating the activation of transcription factors. In organisms, it is synthesized from 1-arginine in the presence of an enzyme called nitric oxide synthase and it can act as a biosignaling molecule. Sulfotransferases (SULTs) are important phase II drug-metabolizing enzymes responsible for drug metabolism and xenobiotics detoxification. SULTs are also important in the regulation and metabolism of endogenous hormones and other important signaling molecules. This report investigates human SULT gene regulation by nitric oxide and the potential molecular mechanisms. Here we report the effect of nitric oxide on the expression of human SULT1A1 and SULT2A1, the two major human SULTs. When Hep G2 cells were treated with diethylene triamine/nitric oxide (DETA/NO), Western blot and q-RT-PCR data suggested that SULT2A1 was downregulated, while SULT1A1 was not significantly affected. The downregulation of SULT2A1 occurred in a time- and concentration-dependent manner. DETA/NO induced the phosphorylation of extracellular signal-regulated protein kinase (ERK). PD98059, a pharmacological inhibitor of ERK, prevented the DETA/NO downregulation of SULT2A1. The present study suggested that the downregulation of SULT2A1 involves ERK cell signaling pathways. This is the first report on nitrative stress regulation of human SULT2A1. The results are important for understanding biological functions of SULTs in organisms under stress.
 
 
 
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