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10.1021/acs.jproteome.7b00107 http://scihub22266oqcxt.onion/10.1021/acs.jproteome.7b00107 C5484408!5484408 !28347137     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28347137 &cmd=llinks): Failed to open stream: HTTP request failed! 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Quantitative Proteomics and Immunohistochemistry Reveal Insights into Cellular and Molecular Processes in the Infarct Border Zone One Month after Myocardial Infarction |pdf=|usr=}}{{28347137 }} gab.com Text Quantitative Proteomics and Immunohistochemistry Reveal Insights into Cellular and Molecular Processes in the Infarct Border Zone One Month after Myocardial Infarction JO: J Proteome Res http://www.kidney.de/pget.php?&tw=1&pmid=28347137 #FOAvip Postinfarction remodeling and expansion of the peri-infarct border zone (BZ) directly correlate with mortality following myocardial infarction (MI); however, the cellular and molecular mechanisms underlying remodeling processes in the BZ remain unclear. Herein, we utilized a label-free quantitative proteomics approach in combination with immunohistochemical analyses to gain a better understanding of processes contributing to postinfarction remodeling of the peri-infarct BZ in a swine model of MI with reperfusion. Our analysis uncovered a significant down-regulation of proteins involved in energy metabolism, indicating impaired myocardial energetics and possibly mitochondrial dysfunction, in the peri-scar BZ. An increase in endothelial and vascular smooth muscles cells, as well as up-regulation of proteins implicated in vascular endothelial growth factor (VEGF) signaling and marked changes in the expression of extracellular matrix and subendothelial basement membrane proteins, is indicative of active angiogenesis in the infarct BZ. A pronounced increase in macrophages in the peri-infarct BZ was also observed, and proteomic analysis uncovered evidence of persistent inflammation in this tissue. Additional evidence suggested an increase in cellular proliferation that, concomitant with increased nestin expression, indicates potential turnover of endogenous stem cells in the BZ. A marked up-regulation of pro-apoptotic proteins, as well as the down-regulation of proteins important for adaptation to mechanical, metabolic, and oxidative stress, likely contributes to increased apoptosis in the peri-infarct BZ. The cellular processes and molecular pathways identified herein may have clinical utility for therapeutic intervention aimed at limiting remodeling and expansion of the BZ myocardium and preventing the development of heart failure post-MI. Twit Text FOAVip Quantitative Proteomics and Immunohistochemistry Reveal Insights into Cellular and Molecular Processes in the Infarct Border Zone One Month after Myocardial Infarction ????J Proteome Res http://www.kidney.de/pget.php?&tw=1&pmid=28347137 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28347137 #FOAvip English Wikipedia <ref>{{Cite pmid|28347137 }}</ref> Quantitative Proteomics and Immunohistochemistry Reveal Insights into Cellular and Molecular Processes in the Infarct Border Zone One Month after Myocardial Infarction #MMPMID28347137 Yang L ; Gregorich ZR ; Cai W ; Zhang P ; Young B ; Gu Y ; Zhang J ; Ge Y J Proteome Res 2017[May]; 16 (5 ): 2101-2112 PMID28347137 show ga Postinfarction remodeling and expansion of the peri-infarct border zone (BZ) directly correlate with mortality following myocardial infarction (MI); however, the cellular and molecular mechanisms underlying remodeling processes in the BZ remain unclear. Herein, we utilized a label-free quantitative proteomics approach in combination with immunohistochemical analyses to gain a better understanding of processes contributing to postinfarction remodeling of the peri-infarct BZ in a swine model of MI with reperfusion. Our analysis uncovered a significant down-regulation of proteins involved in energy metabolism, indicating impaired myocardial energetics and possibly mitochondrial dysfunction, in the peri-scar BZ. An increase in endothelial and vascular smooth muscles cells, as well as up-regulation of proteins implicated in vascular endothelial growth factor (VEGF) signaling and marked changes in the expression of extracellular matrix and subendothelial basement membrane proteins, is indicative of active angiogenesis in the infarct BZ. A pronounced increase in macrophages in the peri-infarct BZ was also observed, and proteomic analysis uncovered evidence of persistent inflammation in this tissue. Additional evidence suggested an increase in cellular proliferation that, concomitant with increased nestin expression, indicates potential turnover of endogenous stem cells in the BZ. A marked up-regulation of pro-apoptotic proteins, as well as the down-regulation of proteins important for adaptation to mechanical, metabolic, and oxidative stress, likely contributes to increased apoptosis in the peri-infarct BZ. The cellular processes and molecular pathways identified herein may have clinical utility for therapeutic intervention aimed at limiting remodeling and expansion of the BZ myocardium and preventing the development of heart failure post-MI. |Animals [MESH] |Apoptosis [MESH] |Energy Metabolism [MESH] |Immunohistochemistry/*methods [MESH] |Inflammation [MESH] |Myocardial Infarction/*metabolism [MESH] |Neovascularization, Pathologic [MESH] |Proteins/analysis [MESH] |Proteomics/*methods [MESH]Quantitative Proteomics and Immunohistochemistry Reveal Insights into (epmc).pdf DeepDyve Pubget Overpricing