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10.1172/JCI82819 http://scihub22266oqcxt.onion/10.1172/JCI82819 C4731189!4731189!26731474     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       J+Clin+Invest ä ; 126 (2): 721-31 Nephropedia Template TP {{tp|p=26731474|t=ä. DNA methyltransferase inhibition restores erythropoietin production in fibrotic murine kidneys |pdf=|usr=}}{{26731474}} gab.com Text DNA methyltransferase inhibition restores erythropoietin production in fibrotic murine kidneys JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26731474 #FOAvip Renal erythropoietin-producing cells (REPCs) remain in the kidneys of patients with chronic kidney disease, but these cells do not produce sufficient erythropoietin in response to hypoxic stimuli. Treatment with HIF stabilizers rescues erythropoietin production in these cells, but the mechanisms underlying the decreased response of REPCs in fibrotic kidneys to anemic stimulation remain elusive. Here, we show that fibroblast-like FOXD1+ progenitor-derived kidney pericytes, which are characterized by the expression of ?1 type I collagen and PDGFR?, produce erythropoietin through HIF2? regulation but that production is repressed when these cells differentiate into myofibroblasts. DNA methyltransferases and erythropoietin hypermethylation are upregulated in myofibroblasts. Exposure of myofibroblasts to nanomolar concentrations of the demethylating agent 5-azacytidine increased basal expression and hypoxic induction of erythropoietin. Mechanistically, the profibrotic factor TGF-?1 induced hypermethylation and repression of erythropoietin in pericytes; these effects were prevented by 5-azacytidine treatment. These findings shed light on the molecular mechanisms underlying erythropoietin repression in kidney myofibroblasts and demonstrate that clinically relevant, nontoxic doses of 5-azacytidine can restore erythropoietin production and ameliorate anemia in the setting of kidney fibrosis in mice. Twit Text FOAVip DNA methyltransferase inhibition restores erythropoietin production in fibrotic murine kidneys ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26731474 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26731474 #FOAvip English Wikipedia <ref>{{Cite pmid|26731474}}</ref> DNA methyltransferase inhibition restores erythropoietin production in fibrotic murine kidneys #MMPMID26731474 Chang YT; Yang CC; Pan SY; Chou YH; Chang FC; Lai CF; Tsai MH; Hsu HL; Lin CH; Chiang WC; Wu MS; Chu TS; Chen YM; Lin SL J Clin Invest ä[]; 126 (2): 721-31 PMID26731474show ga Renal erythropoietin-producing cells (REPCs) remain in the kidneys of patients with chronic kidney disease, but these cells do not produce sufficient erythropoietin in response to hypoxic stimuli. Treatment with HIF stabilizers rescues erythropoietin production in these cells, but the mechanisms underlying the decreased response of REPCs in fibrotic kidneys to anemic stimulation remain elusive. Here, we show that fibroblast-like FOXD1+ progenitor-derived kidney pericytes, which are characterized by the expression of ?1 type I collagen and PDGFR?, produce erythropoietin through HIF2? regulation but that production is repressed when these cells differentiate into myofibroblasts. DNA methyltransferases and erythropoietin hypermethylation are upregulated in myofibroblasts. Exposure of myofibroblasts to nanomolar concentrations of the demethylating agent 5-azacytidine increased basal expression and hypoxic induction of erythropoietin. Mechanistically, the profibrotic factor TGF-?1 induced hypermethylation and repression of erythropoietin in pericytes; these effects were prevented by 5-azacytidine treatment. These findings shed light on the molecular mechanisms underlying erythropoietin repression in kidney myofibroblasts and demonstrate that clinically relevant, nontoxic doses of 5-azacytidine can restore erythropoietin production and ameliorate anemia in the setting of kidney fibrosis in mice. äDNA methyltransferase inhibition restores erythropoietin production in(epmc).pdf DeepDyve Pubget Overpricing