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10.1186/s13287-017-0645-8 http://scihub22266oqcxt.onion/10.1186/s13287-017-0645-8 C5606115!5606115 !28927462     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28927462 &cmd=llinks): Failed to open stream: HTTP request failed! 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Generation of special autosomal dominant polycystic kidney disease iPSCs with the capability of functional kidney-like cell differentiation |pdf=|usr=}}{{28927462 }} gab.com Text Generation of special autosomal dominant polycystic kidney disease iPSCs with the capability of functional kidney-like cell differentiation JO: Stem Cell Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=28927462 #FOAvip BACKGROUND: Human induced pluripotent stem cells (iPSCs) have been verified as a powerful cell model for the study of pathogenesis in hereditary disease. Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations of PKD or non-PKD genes. The pathogenesis of ADPKD remains unexplored because of the lack of a true human cell model. METHODS: Six ADPKD patients and four healthy individuals were recruited as donors of somatic cells from a Chinese ADPKD family without mutations of the PKD genes but carrying SAMSN1 gene deletion. The ADPKD-iPSCs were generated from somatic cells and were induced into kidney-like cells (KLCs) by a novel three-step method involving cytokines and renal epithelium growth medium. Furthermore, we analyzed functional properties of these KLCs by water transportation and albumin absorption assays. RESULTS: We successfully generated iPSCs from ADPKD patients and differentiated them into KLCs that showed morphological and functional characteristics of human kidney cells. Further, we also found that ADPKD-iPSC-KLCs had a significantly higher rate of apoptosis and a significantly lower capacity for water transportation and albumin absorption compared to healthy sibling-derived differentiated KLCs. Furthermore, knockdown of SAMSN1 in control iPSCs may attenuate differentiation and/or function of KLCs. CONCLUSIONS: These data show that we have created the first iPSCs established from ADPKD patients without mutations in the PKD genes, and suggest that the deletion mutation of SAMSN1 might be involved in the differentiation and/or function of KLCs. ADPKD-iPSC-KLCs can be used as a versatile model system for the study of kidney disease. Twit Text FOAVip Generation of special autosomal dominant polycystic kidney disease iPSCs with the capability of functional kidney-like cell differentiation ????Stem Cell Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=28927462 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28927462 #FOAvip English Wikipedia <ref>{{Cite pmid|28927462 }}</ref> Generation of special autosomal dominant polycystic kidney disease iPSCs with the capability of functional kidney-like cell differentiation #MMPMID28927462 Huang J ; Zhou S ; Niu X ; Hu B ; Li Q ; Zhang F ; Zhang X ; Cai X ; Lou Y ; Liu F ; Xu C ; Wang Y Stem Cell Res Ther 2017[Sep]; 8 (1 ): 196 PMID28927462 show ga BACKGROUND: Human induced pluripotent stem cells (iPSCs) have been verified as a powerful cell model for the study of pathogenesis in hereditary disease. Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations of PKD or non-PKD genes. The pathogenesis of ADPKD remains unexplored because of the lack of a true human cell model. METHODS: Six ADPKD patients and four healthy individuals were recruited as donors of somatic cells from a Chinese ADPKD family without mutations of the PKD genes but carrying SAMSN1 gene deletion. The ADPKD-iPSCs were generated from somatic cells and were induced into kidney-like cells (KLCs) by a novel three-step method involving cytokines and renal epithelium growth medium. Furthermore, we analyzed functional properties of these KLCs by water transportation and albumin absorption assays. RESULTS: We successfully generated iPSCs from ADPKD patients and differentiated them into KLCs that showed morphological and functional characteristics of human kidney cells. Further, we also found that ADPKD-iPSC-KLCs had a significantly higher rate of apoptosis and a significantly lower capacity for water transportation and albumin absorption compared to healthy sibling-derived differentiated KLCs. Furthermore, knockdown of SAMSN1 in control iPSCs may attenuate differentiation and/or function of KLCs. CONCLUSIONS: These data show that we have created the first iPSCs established from ADPKD patients without mutations in the PKD genes, and suggest that the deletion mutation of SAMSN1 might be involved in the differentiation and/or function of KLCs. ADPKD-iPSC-KLCs can be used as a versatile model system for the study of kidney disease. |Adaptor Proteins, Vesicular Transport/deficiency/*genetics [MESH] |Adolescent [MESH] |Albumins/metabolism [MESH] |Biological Transport [MESH] |Cell Differentiation [MESH] |Comparative Genomic Hybridization [MESH] |DNA Mutational Analysis [MESH] |Epithelial Cells/*metabolism/pathology [MESH] |Female [MESH] |Gene Deletion [MESH] |Gene Expression [MESH] |Humans [MESH] |Induced Pluripotent Stem Cells/*metabolism/pathology [MESH] |Kidney/*metabolism/pathology [MESH] |Male [MESH] |Middle Aged [MESH] |Nerve Tissue Proteins/deficiency/*genetics [MESH] |Pedigree [MESH] |Polycystic Kidney, Autosomal Dominant/*genetics/metabolism/pathology [MESH] |Primary Cell Culture [MESH] |Receptors, Cell Surface/deficiency/*genetics [MESH] |TRPP Cation Channels/*genetics/metabolism [MESH]Generation of special autosomal dominant polycystic kidney disease iPS(epmc).pdf DeepDyve Pubget Overpricing