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10.1016/j.jacc.2013.11.023 http://scihub22266oqcxt.onion/10.1016/j.jacc.2013.11.023 C3992176!3992176!24361318     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24361318&cmd=llinks): Failed to open stream: HTTP request failed! 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In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing |pdf=|usr=}}{{24361318}} gab.com Text In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing JO: J Am Coll Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=24361318 #FOAvip Objectives: The aim of the study was to test wether silencing of the transcription factor Interferon Regulatory Factor 5 (IRF5) in cardiac macrophages improves infarct healing and attenuates post-MI remodeling. Background: In healing wounds, M1?M2 macrophage phenotype transition supports resolution of inflammation and tissue repair. Persistence of inflammatory M1 macrophages may derail healing and compromise organ functions. The transcription factor IRF5 promotes genes associated with M1 macrophages. Methods: Here we used nanoparticle-delivered siRNA to silence the transcription factor IRF5 in macrophages residing in myocardial infarcts (MI) and in surgically induced skin wounds in mice. Results: Infarct macrophages expressed high levels of IRF5 during the early inflammatory wound healing stages (day 4 after coronary ligation) whereas expression of the transcription factor decreased during the resolution of inflammation (day 8). Following in vitro screening, we identified an siRNA sequence that, when delivered by nanoparticles to wound macrophages, efficiently suppressed expression of IRF5 in vivo. Reduction of IRF5 expression, a factor that regulates macrophage polarization, reduced inflammatory M1 macrophage markers, supported resolution of inflammation, accelerated cutaneous and infarct healing and attenuated development of post-MI heart failure after coronary ligation as measured by protease targeted FMT-CT imaging and cardiac MRI (p<0.05 respectively). Conclusion: This work identifies a new therapeutic avenue to augment resolution of inflammation in healing infarcts by macrophage phenotype manipulation. This therapeutic concept may be used to attenuate post-MI remodeling and heart failure. Twit Text FOAVip In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing ????J Am Coll Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=24361318 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24361318 #FOAvip English Wikipedia <ref>{{Cite pmid|24361318}}</ref> In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing #MMPMID24361318 Courties G; Heidt T; Sebas M; Iwamoto Y; Jeon D; Truelove J; Tricot B; Wojtkiewicz G; Dutta P; Sager HB; Borodovsky A; Novobrantseva T; Klebanov B; Fitzgerald K; Anderson DG; Libby P; Swirski FK; Weissleder R; Nahrendorf M J Am Coll Cardiol 2014[Apr]; 63 (15): 1556-66 PMID24361318show ga Objectives: The aim of the study was to test wether silencing of the transcription factor Interferon Regulatory Factor 5 (IRF5) in cardiac macrophages improves infarct healing and attenuates post-MI remodeling. Background: In healing wounds, M1?M2 macrophage phenotype transition supports resolution of inflammation and tissue repair. Persistence of inflammatory M1 macrophages may derail healing and compromise organ functions. The transcription factor IRF5 promotes genes associated with M1 macrophages. Methods: Here we used nanoparticle-delivered siRNA to silence the transcription factor IRF5 in macrophages residing in myocardial infarcts (MI) and in surgically induced skin wounds in mice. Results: Infarct macrophages expressed high levels of IRF5 during the early inflammatory wound healing stages (day 4 after coronary ligation) whereas expression of the transcription factor decreased during the resolution of inflammation (day 8). Following in vitro screening, we identified an siRNA sequence that, when delivered by nanoparticles to wound macrophages, efficiently suppressed expression of IRF5 in vivo. Reduction of IRF5 expression, a factor that regulates macrophage polarization, reduced inflammatory M1 macrophage markers, supported resolution of inflammation, accelerated cutaneous and infarct healing and attenuated development of post-MI heart failure after coronary ligation as measured by protease targeted FMT-CT imaging and cardiac MRI (p<0.05 respectively). Conclusion: This work identifies a new therapeutic avenue to augment resolution of inflammation in healing infarcts by macrophage phenotype manipulation. This therapeutic concept may be used to attenuate post-MI remodeling and heart failure. äIn vivo silencing of the transcription factor IRF5 reprograms the macr(epmc).pdf DeepDyve Pubget Overpricing