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10.1152/ajprenal.00146.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00146.2014 C4346747!4346747!25537742     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2015 ; 308 (5): F459-72 Nephropedia Template TP {{tp|p=25537742|t=2015. Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors |pdf=|usr=}}{{25537742}} gab.com Text Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25537742 #FOAvip Kidney fibrosis is the final common pathway for virtually every type of chronic kidney disease and is a consequence of a prolonged healing response that follows tissue inflammation. Chronic kidney inflammation ultimately leads to progressive tissue injury and scarring/fibrosis. Several pathways have been implicated in the progression of kidney fibrosis. In the present study, we demonstrate that G protein-coupled chemokine (C-X-C motif) receptor (CXCR)4 was significantly upregulated after renal injury and that sustained activation of Cxcr4 expression augmented the fibrotic response. We demonstrate that after unilateral ureteral obstruction (UUO), both gene and protein expression of Cxcr4 were highly upregulated in tubular cells of the nephron. The increased Cxcr4 expression in tubules correlated with their increased dedifferentiated state, leading to increased mRNA expression of platelet-derived growth factor (PDGF)-?, transforming growth factor (TGF)-?1, and concurrent loss of bone morphogenetic protein 7 (Bmp7). Ablation of tubular Cxcr4 attenuated UUO-mediated fibrotic responses, which correlated with a significant reduction in PDGF-? and TGF-?1 levels and preservation of Bmp7 expression after UUO. Furthermore, Cxcr4+ immune cells infiltrated the obstructed kidney and further upregulate their Cxcr4 expression. Genetic ablation of Cxcr4 from macrophages was protective against UUO-induced fibrosis. There was also reduced total kidney TGF-?1, which correlated with reduced Smad activation and ?-smooth muscle actin levels. We conclude that chronic high Cxcr4 expression in multiple effector cell types can contribute to the pathogenesis of renal fibrosis by altering their biological profile. This study uncovered a novel cross-talk between Cxcr4-TGF-?1 and Bmp7 pathways and may provide novel targets for interrupting the progression of fibrosis. Twit Text FOAVip Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25537742 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25537742 #FOAvip English Wikipedia <ref>{{Cite pmid|25537742}}</ref> Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors #MMPMID25537742 Yuan A; Lee Y; Choi U; Moeckel G; Karihaloo A Am J Physiol Renal Physiol 2015[Mar]; 308 (5): F459-72 PMID25537742show ga Kidney fibrosis is the final common pathway for virtually every type of chronic kidney disease and is a consequence of a prolonged healing response that follows tissue inflammation. Chronic kidney inflammation ultimately leads to progressive tissue injury and scarring/fibrosis. Several pathways have been implicated in the progression of kidney fibrosis. In the present study, we demonstrate that G protein-coupled chemokine (C-X-C motif) receptor (CXCR)4 was significantly upregulated after renal injury and that sustained activation of Cxcr4 expression augmented the fibrotic response. We demonstrate that after unilateral ureteral obstruction (UUO), both gene and protein expression of Cxcr4 were highly upregulated in tubular cells of the nephron. The increased Cxcr4 expression in tubules correlated with their increased dedifferentiated state, leading to increased mRNA expression of platelet-derived growth factor (PDGF)-?, transforming growth factor (TGF)-?1, and concurrent loss of bone morphogenetic protein 7 (Bmp7). Ablation of tubular Cxcr4 attenuated UUO-mediated fibrotic responses, which correlated with a significant reduction in PDGF-? and TGF-?1 levels and preservation of Bmp7 expression after UUO. Furthermore, Cxcr4+ immune cells infiltrated the obstructed kidney and further upregulate their Cxcr4 expression. Genetic ablation of Cxcr4 from macrophages was protective against UUO-induced fibrosis. There was also reduced total kidney TGF-?1, which correlated with reduced Smad activation and ?-smooth muscle actin levels. We conclude that chronic high Cxcr4 expression in multiple effector cell types can contribute to the pathogenesis of renal fibrosis by altering their biological profile. This study uncovered a novel cross-talk between Cxcr4-TGF-?1 and Bmp7 pathways and may provide novel targets for interrupting the progression of fibrosis. äChemokine receptor Cxcr4 contributes to kidney fibrosis via multiple e(epmc).pdf DeepDyve Pubget Overpricing