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10.4161/15384101.2014.949091 http://scihub22266oqcxt.onion/10.4161/15384101.2014.949091 C4612710!4612710 !25486565     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25486565 &cmd=llinks): Failed to open stream: HTTP request failed! 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Different effects of ZO-1, ZO-2 and ZO-3 silencing on kidney collecting duct principal cell proliferation and adhesion |pdf=|usr=}}{{25486565 }} gab.com Text Different effects of ZO-1, ZO-2 and ZO-3 silencing on kidney collecting duct principal cell proliferation and adhesion JO: Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=25486565 #FOAvip Coordinated cell proliferation and ability to form intercellular seals are essential features of epithelial tissue function. Tight junctions (TJs) classically act as paracellular diffusion barriers. More recently, their role in regulating epithelial cell proliferation in conjunction with scaffolding zonula occludens (ZO) proteins has come to light. The kidney collecting duct (CD) is a model of tight epithelium that displays intense proliferation during embryogenesis followed by very low cell turnover in the adult kidney. Here, we examined the influence of each ZO protein (ZO-1, -2 and -3) on CD cell proliferation. We show that all 3 ZO proteins are strongly expressed in native CD and are present at both intercellular junctions and nuclei of cultured CD principal cells (mCCDcl1). Suppression of either ZO-1 or ZO-2 resulted in increased G0/G1 retention in mCCDcl1 cells. ZO-2 suppression decreased cyclin D1 abundance while ZO-1 suppression was accompanied by increased nuclear p21 localization, the depletion of which restored cell cycle progression. Contrary to ZO-1 and ZO-2, ZO-3 expression at intercellular junctions dramatically increased with cell density and relied on the presence of ZO-1. ZO-3 depletion did not affect cell cycle progression but increased cell detachment. This latter event partly relied on increased nuclear cyclin D1 abundance and was associated with altered ?1-integrin subcellular distribution and decreased occludin expression at intercellular junctions. These data reveal diverging, but interconnected, roles for each ZO protein in mCCDcl1 proliferation. While ZO-1 and ZO-2 participate in cell cycle progression, ZO-3 is an important component of cell adhesion. Twit Text FOAVip Different effects of ZO-1, ZO-2 and ZO-3 silencing on kidney collecting duct principal cell proliferation and adhesion ????Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=25486565 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25486565 #FOAvip English Wikipedia <ref>{{Cite pmid|25486565 }}</ref> Different effects of ZO-1, ZO-2 and ZO-3 silencing on kidney collecting duct principal cell proliferation and adhesion #MMPMID25486565 Qiao X ; Roth I ; Féraille E ; Hasler U Cell Cycle 2014[]; 13 (19 ): 3059-75 PMID25486565 show ga Coordinated cell proliferation and ability to form intercellular seals are essential features of epithelial tissue function. Tight junctions (TJs) classically act as paracellular diffusion barriers. More recently, their role in regulating epithelial cell proliferation in conjunction with scaffolding zonula occludens (ZO) proteins has come to light. The kidney collecting duct (CD) is a model of tight epithelium that displays intense proliferation during embryogenesis followed by very low cell turnover in the adult kidney. Here, we examined the influence of each ZO protein (ZO-1, -2 and -3) on CD cell proliferation. We show that all 3 ZO proteins are strongly expressed in native CD and are present at both intercellular junctions and nuclei of cultured CD principal cells (mCCDcl1). Suppression of either ZO-1 or ZO-2 resulted in increased G0/G1 retention in mCCDcl1 cells. ZO-2 suppression decreased cyclin D1 abundance while ZO-1 suppression was accompanied by increased nuclear p21 localization, the depletion of which restored cell cycle progression. Contrary to ZO-1 and ZO-2, ZO-3 expression at intercellular junctions dramatically increased with cell density and relied on the presence of ZO-1. ZO-3 depletion did not affect cell cycle progression but increased cell detachment. This latter event partly relied on increased nuclear cyclin D1 abundance and was associated with altered ?1-integrin subcellular distribution and decreased occludin expression at intercellular junctions. These data reveal diverging, but interconnected, roles for each ZO protein in mCCDcl1 proliferation. While ZO-1 and ZO-2 participate in cell cycle progression, ZO-3 is an important component of cell adhesion. |*RNA Interference [MESH] |Animals [MESH] |Cell Adhesion [MESH] |Cell Cycle Checkpoints [MESH] |Cell Proliferation [MESH] |Cells, Cultured [MESH] |Cyclin D1/metabolism [MESH] |Cyclin-Dependent Kinase Inhibitor p21/metabolism [MESH] |Kidney Tubules, Collecting/*cytology/metabolism [MESH] |Proliferating Cell Nuclear Antigen/metabolism [MESH] |RNA, Messenger/metabolism [MESH] |RNA, Small Interfering/metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Zonula Occludens Proteins/antagonists & inhibitors/genetics/*metabolism [MESH] |Zonula Occludens-1 Protein/antagonists & inhibitors/genetics/*metabolism [MESH]Different effects of ZO-1, ZO-2 and ZO-3 silencing on kidney collectin(epmc).pdf DeepDyve Pubget Overpricing