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10.1016/j.cmet.2015.09.012 http://scihub22266oqcxt.onion/10.1016/j.cmet.2015.09.012 C4635034!4635034 !26456334     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 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 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 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26456334 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Metab 2015 ; 22 (5 ): 799-810 Nephropedia Template TP {{tp|p=26456334 |t=2015. IL-17A Is Increased in Humans with Primary Hyperparathyroidism and Mediates PTH-Induced Bone Loss in Mice |pdf=|usr=}}{{26456334 }} gab.com Text IL-17A Is Increased in Humans with Primary Hyperparathyroidism and Mediates PTH-Induced Bone Loss in Mice JO: Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=26456334 #FOAvip Primary hyperparathyroidism (PHPT) is a common cause of bone loss that is modeled by continuous PTH (cPTH) infusion. Here we show that the inflammatory cytokine IL-17A is upregulated by PHPT in humans and cPTH in mice. In humans, IL-17A is normalized by parathyroidectomy. In mice, treatment with anti-IL-17A antibody and silencing of IL-17A receptor IL-17RA prevent cPTH-induced osteocytic and osteoblastic RANKL production and bone loss. Mechanistically, cPTH stimulates conventional T cell production of TNF? (TNF), which increases the differentiation of IL-17A-producing Th17 cells via TNF receptor 1 (TNFR1) signaling in CD4(+) cells. Moreover, cPTH enhances the sensitivity of naive CD4(+) cells to TNF via G?S/cAMP/Ca(2+) signaling. Accordingly, conditional deletion of G?S in CD4(+) cells and treatment with the calcium channel blocker diltiazem prevents Th17 cell expansion and blocks cPTH-induced bone loss. Neutralization of IL-17A and calcium channel blockers may thus represent novel therapeutic strategies for hyperparathyroidism. Twit Text FOAVip IL-17A Is Increased in Humans with Primary Hyperparathyroidism and Mediates PTH-Induced Bone Loss in Mice ????Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=26456334 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26456334 #FOAvip English Wikipedia <ref>{{Cite pmid|26456334 }}</ref> IL-17A Is Increased in Humans with Primary Hyperparathyroidism and Mediates PTH-Induced Bone Loss in Mice #MMPMID26456334 Li JY ; D'Amelio P ; Robinson J ; Walker LD ; Vaccaro C ; Luo T ; Tyagi AM ; Yu M ; Reott M ; Sassi F ; Buondonno I ; Adams J ; Weitzmann MN ; Isaia GC ; Pacifici R Cell Metab 2015[Nov]; 22 (5 ): 799-810 PMID26456334 show ga Primary hyperparathyroidism (PHPT) is a common cause of bone loss that is modeled by continuous PTH (cPTH) infusion. Here we show that the inflammatory cytokine IL-17A is upregulated by PHPT in humans and cPTH in mice. In humans, IL-17A is normalized by parathyroidectomy. In mice, treatment with anti-IL-17A antibody and silencing of IL-17A receptor IL-17RA prevent cPTH-induced osteocytic and osteoblastic RANKL production and bone loss. Mechanistically, cPTH stimulates conventional T cell production of TNF? (TNF), which increases the differentiation of IL-17A-producing Th17 cells via TNF receptor 1 (TNFR1) signaling in CD4(+) cells. Moreover, cPTH enhances the sensitivity of naive CD4(+) cells to TNF via G?S/cAMP/Ca(2+) signaling. Accordingly, conditional deletion of G?S in CD4(+) cells and treatment with the calcium channel blocker diltiazem prevents Th17 cell expansion and blocks cPTH-induced bone loss. Neutralization of IL-17A and calcium channel blockers may thus represent novel therapeutic strategies for hyperparathyroidism. |Animals [MESH] |Bone Diseases, Metabolic/drug therapy/etiology/*metabolism/pathology [MESH] |Calcium Channel Blockers/therapeutic use [MESH] |Humans [MESH] |Hyperparathyroidism, Primary/complications/drug therapy/*metabolism/pathology [MESH] |Interleukin-17/biosynthesis/*metabolism [MESH] |Mice [MESH] |Receptors, Tumor Necrosis Factor, Type I/biosynthesis [MESH] |Signal Transduction [MESH] |T-Lymphocytes/metabolism/pathology [MESH]IL-17A Is Increased in Humans with Primary Hyperparathyroidism and Med(epmc).pdf DeepDyve Pubget Overpricing