Maureen Voller

NL Agency, Netherlands, 's-Gravenhage, South Holland, Netherlands

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Publications (6)24.11 Total impact

  • European Urology Supplements; 09/2006
  • European Urology Supplements 09/2006; 5(14):792-792. DOI:10.1016/S1569-9056(06)61274-8 · 3.37 Impact Factor
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    ABSTRACT: Prostate cancer is the most commonly diagnosed type of cancer in men, and there is no available cure for patients with advanced disease. In vitro model systems are urgently required to permit the study of human prostate cell differentiation and malignant transformation. Unfortunately, human prostate cells are particularly difficult to convert into continuously growing cultures. We report here the successful immortalization without viral oncogenes of prostate epithelial cells and, for the first time, prostate stromal cells. These cells exhibit a significant pattern of authentic prostate-specific features. In particular, the epithelial cell culture is able to differentiate into glandular buds that closely resemble the structures formed by primary prostate epithelial cells. The stromal cells have typical characteristics of prostate smooth muscle cells. These immortalized cultures may serve as a unique experimental platform to permit several research directions, including the study of cell-cell interactions in an authentic prostate microenvironment, prostate cell differentiation, and most significantly, the complex multistep process leading to prostate cell transformation.
    Cancer Research 05/2006; 66(7):3531-40. DOI:10.1158/0008-5472.CAN-05-2183 · 9.28 Impact Factor
  • European Urology Supplements; 04/2006
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    ABSTRACT: We have compared the agonist-induced down-regulation of human alpha1A-, alpha1B- and alpha1D-adrenoceptors upon stable expression in rat-1 fibroblasts. During a 24-h incubation the agonist phenylephrine downregulated alpha1A- and alpha1 -adrenoceptors in a concentration-dependent manner. While maximum downregulation was similar for both subtypes, the threshold concentration for significant reductions was markedly higher for alpha1A- than for alpha(1B-adrenoceptors (10 microM vs. 100 nM). The downregulation of both subtypes by 100 microM phenylephrine was time-dependent, and significant reductions were observed already after 2-4 h. In contrast, incubation of alpha1D-adrenoceptor-expressing cells with phenylephrine increased receptor number in a time- and concentration-dependent manner. The downregulation of alpha1B-adrenoceptors by 100 microM phenylephrine for 24 h was accompanied by a matching reduction in mRNA abundance, but no such reduction was seen for alpha-adrenoceptors. These treatment conditions also caused a functional desensitization of agonist-stimulated inositol phosphate formation for alpha1A- and alpha1B- but not for alpha1D-adrenoceptors. Treatment with the phorbol ester phorbol-12-myristate-13-acetate did not change receptor density or mRNA abundance and did not cause functional desensitization. We conclude that human alpha1-adrenoceptor subtypes are differentially regulated by agonist treatment even if they are expressed in the same cell line.
    Archiv für Experimentelle Pathologie und Pharmakologie 07/1999; 359(6):439-46. · 2.36 Impact Factor
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    ABSTRACT: We have compared the agonist-induced downregulation of human α1A-, α1B- and α1D-adrenoceptors upon stable expression in rat-1 fibroblasts. During a 24-h incubation the agonist phenylephrine downregulated α1A- and α1B-adrenoceptors in a concentration-dependent manner. While maximum downregulation was similar for both subtypes, the threshold concentration for significant reductions was markedly higher for α1A- than for α1B-adrenoceptors (10 μM vs. 100 nM). The downregulation of both subtypes by 100 μM phenylephrine was time-dependent, and significant reductions were observed already after 2– 4 h. In contrast, incubation of α1D-adrenoceptor-expressing cells with phenylephrine increased receptor number in a time- and concentration-dependent manner. The downregulation of α1B-adrenoceptors by 100 μM phenylephrine for 24 h was accompanied by a matching reduction in mRNA abundance, but no such reduction was seen for α1A-adrenoceptors. These treatment conditions also caused a functional desensitization of agonist-stimulated inositol phosphate formation for α1A- and α1B- but not for α1D-adrenoceptors. Treatment with the phorbol ester phorbol-12-myristate-13-acetate did not change receptor density or mRNA abundance and did not cause functional desensitization. We conclude that human α1-adrenoceptor subtypes are differentially regulated by agonist treatment even if they are expressed in the same cell line.
    Archiv für Experimentelle Pathologie und Pharmakologie 05/1999; 359(6):439-446. DOI:10.1007/PL00005373 · 2.36 Impact Factor