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Articles by C Perry
Total Records ( 2 ) for C Perry
  N Matigian , G Abrahamsen , R Sutharsan , A. L Cook , A. M Vitale , A Nouwens , B Bellette , J An , M Anderson , A. G Beckhouse , M Bennebroek , R Cecil , A. M Chalk , J Cochrane , Y Fan , F Feron , R McCurdy , J. J McGrath , W Murrell , C Perry , J Raju , S Ravishankar , P. A Silburn , G. T Sutherland , S Mahler , G. D Mellick , S. A Wood , C. M Sue , C. A Wells and A. Mackay Sim
  Nicholas Matigian, Greger Abrahamsen, Ratneswary Sutharsan, Anthony L. Cook, Alejandra M. Vitale, Amanda Nouwens, Bernadette Bellette, Jiyuan An, Matthew Anderson, Anthony G. Beckhouse, Maikel Bennebroek, Rowena Cecil, Alistair M. Chalk, Julie Cochrane, Yongjun Fan, Francois Feron, Richard McCurdy, John J. McGrath, Wayne Murrell, Chris Perry, Jyothy Raju, Sugandha Ravishankar, Peter A. Silburn, Greg T. Sutherland, Stephen Mahler, George D. Mellick, Stephen A. Wood, Carolyn M. Sue, Christine A. Wells, and Alan Mackay-Sim There is a pressing need for patient-derived cell models of brain diseases that are relevant and robust enough to produce the large quantities of cells required for molecular and functional analyses. We describe here a new cell model based on patient-derived cells from the human olfactory mucosa, the organ of smell, which regenerates throughout life from neural stem cells. Olfactory mucosa biopsies were obtained from healthy controls and patients with either schizophrenia, a neurodevelopmental psychiatric disorder, or Parkinson’s disease, a neurodegenerative disease. Biopsies were dissociated and grown as neurospheres in defined medium. Neurosphere-derived cell lines were grown in serum-containing medium as adherent monolayers and stored frozen. By comparing 42 patient and control cell lines we demonstrated significant disease-specific alterations in gene expression, protein expression and cell function, including dysregulated neurodevelopmental pathways in schizophrenia and dysregulated mitochondrial function, oxidative stress and xenobiotic metabolism in Parkinson’s disease. The study has identified new candidate genes and cell pathways for future investigation. Fibroblasts from schizophrenia patients did not show these differences. Olfactory neurosphere-derived cells have many advantages over embryonic stem cells and induced pluripotent stem cells as models for brain diseases. They do not require genetic reprogramming and they can be obtained from adults with complex genetic diseases. They will be useful for understanding disease aetiology, for diagnostics and for drug discovery.

  C Perry , O. J Baker , M. E Reyland and I. I. Grichtchenko
 

We examined membrane trafficking of NBCe1-A and NBCe1-B variants of the electrogenic Na+-HCO3 cotransporter (NBCe1) encoded by the SLC4A4 gene, using confocal fluorescent microscopy in rat parotid acinar cells (ParC5 and ParC10). We showed that yellow fluorescent protein (YFP)-tagged NBCe1-A and green fluorescent protein (GFP)-tagged NBCe1-B are colocalized with E-cadherin in the basolateral membrane (BLM) but not with the apical membrane marker zona occludens 1 (ZO-1). We inhibited constitutive recycling with monensin and W13 and detected that NBCe1-A and NBCe1-B accumulated in vesicles marked with the early endosomal marker early endosome antigen-1 (EEA1), with a parallel loss from the BLM. We observed that NBCe1-A and NBCe1-B undergo massive carbachol (CCh)-stimulated redistribution from the BLM into early endosomes. We showed that internalization of NBCe1-A and NBCe1-B was prevented by the general PKC inhibitor GF-109203X, the PKCβ-specific inhibitor Gö-6976, and the PKC-specific inhibitor rottlerin. We verified the involvement of PKC by blocking CCh-induced internalization of NBCe1-A-cyan fluorescent protein (CFP) in cells transfected with dominant-negative kinase-dead (Lys376Arg) PKC-GFP. Our data suggest that NBCe1-A and NBCe1-B undergo constitutive and CCh-stimulated endocytosis regulated by conventional PKCs (PKCβ) and by novel PKC in rat epithelial cells. To help develop a more complete model of the role of NBCe1 in parotid acinar cells we also investigated the initial phase of the secretory response to cholinergic agonist. In an Ussing chamber study we showed that inhibition of basolateral NBCe1 with 5-chloro-2,3-dihydro-3-(hydroxy-2-thienylmethylene)-2-oxo-1H-indole-1-carboxamide (tenidap) significantly decreases an initial phase of luminal anion secretion measured as a transient short-circuit current (Isc) across ParC10 cell monolayers. Using trafficking and functional data we propose a model that describes a physiological role of NBC in salivary acinar cell secretion.

 
 
 
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