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10.1371/journal.pone.0131677 http://scihub22266oqcxt.onion/10.1371/journal.pone.0131677 C4489886!4489886 !26136112     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26136112 &cmd=llinks): Failed to open stream: HTTP request failed! 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Improved Structure and Function in Autosomal Recessive Polycystic Rat Kidneys with Renal Tubular Cell Therapy |pdf=|usr=}}{{26136112 }} gab.com Text Improved Structure and Function in Autosomal Recessive Polycystic Rat Kidneys with Renal Tubular Cell Therapy JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26136112 #FOAvip Autosomal recessive polycystic kidney disease is a truly catastrophic monogenetic disease, causing death and end stage renal disease in neonates and children. Using PCK female rats, an orthologous model of autosomal recessive polycystic kidney disease harboring mutant Pkhd1, we tested the hypothesis that intravenous renal cell transplantation with normal Sprague Dawley male kidney cells would improve the polycystic kidney disease phenotype. Cytotherapy with renal cells expressing wild type Pkhd1 and tubulogenic serum amyloid A1 had powerful and sustained beneficial effects on renal function and structure in the polycystic kidney disease model. Donor cell engraftment and both mutant and wild type Pkhd1 were found in treated but not control PCK kidneys 15 weeks after the final cell infusion. To examine the mechanisms of global protection with a small number of transplanted cells, we tested the hypothesis that exosomes derived from normal Sprague Dawley cells can limit the cystic phenotype of PCK recipient cells. We found that renal exosomes originating from normal Sprague Dawley cells carried and transferred wild type Pkhd1 mRNA to PCK cells in vivo and in vitro and restricted cyst formation by cultured PCK cells. The results indicate that transplantation with renal cells containing wild type Pkhd1 improves renal structure and function in autosomal recessive polycystic kidney disease and may provide an intra-renal supply of normal Pkhd1 mRNA. Twit Text FOAVip Improved Structure and Function in Autosomal Recessive Polycystic Rat Kidneys with Renal Tubular Cell Therapy ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26136112 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26136112 #FOAvip English Wikipedia <ref>{{Cite pmid|26136112 }}</ref> Improved Structure and Function in Autosomal Recessive Polycystic Rat Kidneys with Renal Tubular Cell Therapy #MMPMID26136112 Kelly KJ ; Zhang J ; Han L ; Kamocka M ; Miller C ; Gattone VH 2nd ; Dominguez JH PLoS One 2015[]; 10 (7 ): e0131677 PMID26136112 show ga Autosomal recessive polycystic kidney disease is a truly catastrophic monogenetic disease, causing death and end stage renal disease in neonates and children. Using PCK female rats, an orthologous model of autosomal recessive polycystic kidney disease harboring mutant Pkhd1, we tested the hypothesis that intravenous renal cell transplantation with normal Sprague Dawley male kidney cells would improve the polycystic kidney disease phenotype. Cytotherapy with renal cells expressing wild type Pkhd1 and tubulogenic serum amyloid A1 had powerful and sustained beneficial effects on renal function and structure in the polycystic kidney disease model. Donor cell engraftment and both mutant and wild type Pkhd1 were found in treated but not control PCK kidneys 15 weeks after the final cell infusion. To examine the mechanisms of global protection with a small number of transplanted cells, we tested the hypothesis that exosomes derived from normal Sprague Dawley cells can limit the cystic phenotype of PCK recipient cells. We found that renal exosomes originating from normal Sprague Dawley cells carried and transferred wild type Pkhd1 mRNA to PCK cells in vivo and in vitro and restricted cyst formation by cultured PCK cells. The results indicate that transplantation with renal cells containing wild type Pkhd1 improves renal structure and function in autosomal recessive polycystic kidney disease and may provide an intra-renal supply of normal Pkhd1 mRNA. |Animals [MESH] |Cell Proliferation/drug effects [MESH] |Cell- and Tissue-Based Therapy [MESH] |Cells, Cultured [MESH] |Cysts/metabolism [MESH] |Disease Models, Animal [MESH] |Exosomes [MESH] |Female [MESH] |Genotype [MESH] |Immunohistochemistry [MESH] |In Situ Hybridization, Fluorescence [MESH] |Kidney Tubules/*pathology [MESH] |Liver/metabolism [MESH] |Male [MESH] |Phenotype [MESH] |Polycystic Kidney, Autosomal Recessive/*metabolism/*therapy [MESH] |RNA, Messenger/metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Receptors, Cell Surface/genetics/metabolism [MESH]Improved Structure and Function in Autosomal Recessive Polycystic Rat (epmc).pdf DeepDyve Pubget Overpricing