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10.1111/jcmm.12248 http://scihub22266oqcxt.onion/10.1111/jcmm.12248 C4508142!4508142 !24571348     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24571348 &cmd=llinks): Failed to open stream: HTTP request failed! 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Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis |pdf=|usr=}}{{24571348 }} gab.com Text Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=24571348 #FOAvip We examined whether a shift in macrophage phenotype could be therapeutic for myocardial infarction (MI). The mouse macrophage cell line RAW264.7 was stimulated with peptidoglycan (PGN), with or without 5-azacytidine (5AZ) treatment. MI was induced by ligation of the left anterior descending coronary artery in rats, and the rats were divided into two groups; a saline-injection group and a 5AZ-injection group (2.5 mg/kg/day, intraperitoneal injection). LV function was evaluated and immunohistochemical analyses were performed 2 weeks after MI. Cardiac fibrosis was induced by angiotensin II (AngII) infusion with or without 5AZ (5 mg/kg/day) in mice. Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment. Both induction of inducible nitric oxide synthase (iNOS) and iNOS promoter activity by PGN were inhibited by 5AZ. Ejection fraction (59.00 ± 8.03% versus 42.52 ± 2.58%), contractility (LV dP/dt-max, 8299.76 ± 411.56 mmHg versus 6610.36 ± 282.37 mmHg) and relaxation indices (LV dP/dt-min, -4661.37 ± 210.73 mmHg versus -4219.50 ± 162.98 mmHg) were improved after 5AZ administration. Cardiac fibrosis in the MI+5AZ was 8.14 ± 1.00%, compared with 14.93 ± 2.98% in the MI group (P < 0.05). Arginase-1(+)CD68(+) macrophages with anti-inflammatory phenotype were predominant in the infarct border zone of the MI+5AZ group, in comparison with the MI group. AngII-induced cardiac fibrosis was also attenuated after 5AZ administration. In cardiac fibroblasts, pro-fibrotic mediators and cell proliferation were increased by AngII, and these increases were attenuated after 5AZ treatment. 5AZ exerts its cardiac protective role through modulation of macrophages and cardiac fibroblasts. Twit Text FOAVip Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=24571348 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24571348 #FOAvip English Wikipedia <ref>{{Cite pmid|24571348 }}</ref> Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis #MMPMID24571348 Kim YS ; Kang WS ; Kwon JS ; Hong MH ; Jeong HY ; Jeong HC ; Jeong MH ; Ahn Y J Cell Mol Med 2014[Jun]; 18 (6 ): 1018-27 PMID24571348 show ga We examined whether a shift in macrophage phenotype could be therapeutic for myocardial infarction (MI). The mouse macrophage cell line RAW264.7 was stimulated with peptidoglycan (PGN), with or without 5-azacytidine (5AZ) treatment. MI was induced by ligation of the left anterior descending coronary artery in rats, and the rats were divided into two groups; a saline-injection group and a 5AZ-injection group (2.5 mg/kg/day, intraperitoneal injection). LV function was evaluated and immunohistochemical analyses were performed 2 weeks after MI. Cardiac fibrosis was induced by angiotensin II (AngII) infusion with or without 5AZ (5 mg/kg/day) in mice. Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment. Both induction of inducible nitric oxide synthase (iNOS) and iNOS promoter activity by PGN were inhibited by 5AZ. Ejection fraction (59.00 ± 8.03% versus 42.52 ± 2.58%), contractility (LV dP/dt-max, 8299.76 ± 411.56 mmHg versus 6610.36 ± 282.37 mmHg) and relaxation indices (LV dP/dt-min, -4661.37 ± 210.73 mmHg versus -4219.50 ± 162.98 mmHg) were improved after 5AZ administration. Cardiac fibrosis in the MI+5AZ was 8.14 ± 1.00%, compared with 14.93 ± 2.98% in the MI group (P < 0.05). Arginase-1(+)CD68(+) macrophages with anti-inflammatory phenotype were predominant in the infarct border zone of the MI+5AZ group, in comparison with the MI group. AngII-induced cardiac fibrosis was also attenuated after 5AZ administration. In cardiac fibroblasts, pro-fibrotic mediators and cell proliferation were increased by AngII, and these increases were attenuated after 5AZ treatment. 5AZ exerts its cardiac protective role through modulation of macrophages and cardiac fibroblasts. |Animals [MESH] |Antimetabolites, Antineoplastic/pharmacology [MESH] |Azacitidine/*pharmacology [MESH] |Blotting, Western [MESH] |Cells, Cultured [MESH] |Fibroblasts/drug effects/metabolism/pathology [MESH] |Fibrosis/metabolism/pathology/*prevention & control [MESH] |Immunoenzyme Techniques [MESH] |Macrophages/drug effects/metabolism/*pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Myocardial Infarction/metabolism/pathology/*prevention & control [MESH] |Nitric Oxide Synthase/metabolism [MESH] |Nitric Oxide/*metabolism [MESH] |Peptidoglycan/pharmacology [MESH] |Phenotype [MESH] |RNA, Messenger/genetics [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Ventricular Dysfunction, Left/*drug therapy/metabolism/pathology [MESH]Protective role of 5-azacytidine on myocardial infarction is associate(epmc).pdf DeepDyve Pubget Overpricing