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10.1038/srep13953 http://scihub22266oqcxt.onion/10.1038/srep13953 C4568516!4568516!26365984     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2015 ; 5 (ä): ä Nephropedia Template TP {{tp|p=26365984|t=2015. IP3R deficit underlies loss of salivary fluid secretion in Sjögren?s Syndrome |pdf=|usr=}}{{26365984}} gab.com Text IP3R deficit underlies loss of salivary fluid secretion in Sjögren s Syndrome JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365984 #FOAvip The autoimmune exocrinopathy, Sjögren?s syndrome (SS), is associated with secretory defects in patients, including individuals with mild lymphocytic infiltration and minimal glandular damage. The mechanism(s) underlying the secretory dysfunction is not known. We have used minor salivary gland biopsies from SS patients and healthy individuals to assess acinar cell function in morphologically intact glandular areas. We report that agonist-regulated intracellular Ca2+ release, critically required for Ca2+ entry and fluid secretion, is defective in acini from SS patients. Importantly, these acini displayed reduction in IP3R2 and IP3R3, but not AQP5 or STIM1. Similar decreases in IP3R and carbachol (CCh)-stimulated [Ca2+]i elevation were detected in acinar cells from lymphotoxin-alpha (LT?) transgenic (TG) mice, a model for (SS). Treatment of salivary glands from healthy individuals with LT ?, a cytokine linked to disease progression in SS and IL14? mice, reduced Ca2+ signaling. Together, our findings reveal novel IP3R deficits in acinar cells that underlie secretory dysfunction in SS patients. Twit Text FOAVip IP3R deficit underlies loss of salivary fluid secretion in Sjögren s Syndrome ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365984 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26365984 #FOAvip English Wikipedia <ref>{{Cite pmid|26365984}}</ref> IP3R deficit underlies loss of salivary fluid secretion in Sjögren?s Syndrome #MMPMID26365984 Teos LY; Zhang Y; Cotrim AP; Swaim W; Won JH; Ambrus J; Shen L; Bebris L; Grisius M; Jang SI; Yule DI; Ambudkar IS; Alevizos I Sci Rep 2015[]; 5 (ä): ä PMID26365984show ga The autoimmune exocrinopathy, Sjögren?s syndrome (SS), is associated with secretory defects in patients, including individuals with mild lymphocytic infiltration and minimal glandular damage. The mechanism(s) underlying the secretory dysfunction is not known. We have used minor salivary gland biopsies from SS patients and healthy individuals to assess acinar cell function in morphologically intact glandular areas. We report that agonist-regulated intracellular Ca2+ release, critically required for Ca2+ entry and fluid secretion, is defective in acini from SS patients. Importantly, these acini displayed reduction in IP3R2 and IP3R3, but not AQP5 or STIM1. Similar decreases in IP3R and carbachol (CCh)-stimulated [Ca2+]i elevation were detected in acinar cells from lymphotoxin-alpha (LT?) transgenic (TG) mice, a model for (SS). Treatment of salivary glands from healthy individuals with LT ?, a cytokine linked to disease progression in SS and IL14? mice, reduced Ca2+ signaling. Together, our findings reveal novel IP3R deficits in acinar cells that underlie secretory dysfunction in SS patients. äIP3R deficit underlies loss of salivary fluid secretion in Sjögren?s S(epmc).pdf DeepDyve Pubget Overpricing