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10.1161/CIRCHEARTFAILURE.114.001893 http://scihub22266oqcxt.onion/10.1161/CIRCHEARTFAILURE.114.001893 C4366299!4366299!25550440     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circ+Heart+Fail 2015 ; 8 (2): 352-61 Nephropedia Template TP {{tp|p=25550440|t=2015. Tumor Necrosis Factor: A Mechanistic Link between Angiotensin-II-Induced Cardiac Inflammation and Fibrosis |pdf=|usr=}}{{25550440}} gab.com Text Tumor Necrosis Factor: A Mechanistic Link between Angiotensin-II-Induced Cardiac Inflammation and Fibrosis JO: Circ Heart Fail http://www.kidney.de/pget.php?&tw=1&pmid=25550440 #FOAvip Background: Continuous angiotensin-II (Ang-II) infusion induced the uptake of monocytic fibroblast precursors that initiated the development of cardiac fibrosis; these cells and concurrent fibrosis were absent in mice lacking tumor necrosis factor-alpha receptor 1 (TNFR1). We now investigated their cellular origin and temporal uptake, and the involvement of TNFR1 in monocyte-to-fibroblast differentiation. Methods and Results: Within a day, Ang-II induced a pro-inflammatory environment characterized by production of inflammatory chemokines, cytokines, and TH1-interleukins and uptake of bone marrow-derived M1-cells. After a week, the cardiac environment changed to profibrotic with growth-factor and TH2-interleukin synthesis, uptake of bone marrow-derived M2-cells, and presence of M2-related fibroblasts. TNFR1 signaling was not necessary for early M1 uptake, but its absence diminished the amount of M2-cells. TNFR1-KO hearts also showed reduced levels of cytokine expression, but not of TH-related lymphokines. Reconstitution of wild-type bone marrow into TNFR1-KO mice was sufficient to restore M2 uptake, upregulation of pro-inflammatory and pro-fibrotic genes, and development of fibrosis in response to Ang-II. We also developed an in vitro mouse monocyte-to-fibroblast-maturation assay that confirmed the essential role of TNFR1 in the sequential progression of monocyte activation and fibroblast formation. Conclusions: Development of cardiac fibrosis in response to Ang-II was mediated by myeloid precursors and consisted of two stages. A primary M1 inflammatory response was followed by a subsequent M2 fibrotic response. While the first phase appeared to be independent of TNFR1 signaling, the later phase (and development of fibrosis) was abrogated by deletion of TNFR1. Twit Text FOAVip Tumor Necrosis Factor: A Mechanistic Link between Angiotensin-II-Induced Cardiac Inflammation and Fibrosis ????Circ Heart Fail http://www.kidney.de/pget.php?&tw=1&pmid=25550440 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25550440 #FOAvip English Wikipedia <ref>{{Cite pmid|25550440}}</ref> Tumor Necrosis Factor: A Mechanistic Link between Angiotensin-II-Induced Cardiac Inflammation and Fibrosis #MMPMID25550440 Duerrschmid C; Trial J; Wang Y; Entman ML; Haudek SB Circ Heart Fail 2015[Mar]; 8 (2): 352-61 PMID25550440show ga Background: Continuous angiotensin-II (Ang-II) infusion induced the uptake of monocytic fibroblast precursors that initiated the development of cardiac fibrosis; these cells and concurrent fibrosis were absent in mice lacking tumor necrosis factor-alpha receptor 1 (TNFR1). We now investigated their cellular origin and temporal uptake, and the involvement of TNFR1 in monocyte-to-fibroblast differentiation. Methods and Results: Within a day, Ang-II induced a pro-inflammatory environment characterized by production of inflammatory chemokines, cytokines, and TH1-interleukins and uptake of bone marrow-derived M1-cells. After a week, the cardiac environment changed to profibrotic with growth-factor and TH2-interleukin synthesis, uptake of bone marrow-derived M2-cells, and presence of M2-related fibroblasts. TNFR1 signaling was not necessary for early M1 uptake, but its absence diminished the amount of M2-cells. TNFR1-KO hearts also showed reduced levels of cytokine expression, but not of TH-related lymphokines. Reconstitution of wild-type bone marrow into TNFR1-KO mice was sufficient to restore M2 uptake, upregulation of pro-inflammatory and pro-fibrotic genes, and development of fibrosis in response to Ang-II. We also developed an in vitro mouse monocyte-to-fibroblast-maturation assay that confirmed the essential role of TNFR1 in the sequential progression of monocyte activation and fibroblast formation. Conclusions: Development of cardiac fibrosis in response to Ang-II was mediated by myeloid precursors and consisted of two stages. A primary M1 inflammatory response was followed by a subsequent M2 fibrotic response. While the first phase appeared to be independent of TNFR1 signaling, the later phase (and development of fibrosis) was abrogated by deletion of TNFR1. äTumor Necrosis Factor: A Mechanistic Link between Angiotensin-II-Induc(epmc).pdf DeepDyve Pubget Overpricing