Abstract:
BACKGROUND:Patient outcomes after acute myocardial infarction (AMI) are influenced by the combined activation of several distinct interrelated signaling pathways. Specifically acute-phase response proteins can neutralize inflammatory agents, minimize the extent of tissue damage, and participate in tissue repair and regeneration. We have investigated the evolution of immune response and complement system-related proteins in the early and late phase post-AMI and their potential association with tissue damage after the ischemic event. METHODS:Serum was analyzed by 2D-electrophoresis and mass-spectrometry (MALDI-TOF/TOF) in controls and de novo AMI-patients within the first 6h after onset (admission time), and 3 days after. RESULTS:Among differential proteins two functional groups showed coordinated changes: immune response-inflammation (alpha-1B-glycoprotein, fetuin-A, serum amyloid P-component (SAP), and complex-forming glycoprotein HC) and complement system (C1r, C3 and factor-B). Immune-related proteins showed a decrease 3 days after admission except for SAP that depicted a progressive increase from the early phase. Specifically, fetuin-A decrease was associated with the extent of myocardial necrosis. C1r and C3 were increased in the early phase with a subsequent decrease 3 days after, being C1r levels at admission correlated with necrosis and troponin-T and GPT levels. Contrarily, factor-B was decreased in the early and late phase post-AMI. CONCLUSIONS:Our results demonstrate that in the late phase post-AMI there is a coordinated decrease in immune response-inflammation proteins, except for SAP which showed an increase related to the specific activation of the classical complement pathway. Changes in immunity and complement-related proteins affect the severity of organ damage influencing prognosis after AMI.
journal_name
Int J Cardioljournal_title
International journal of cardiologyauthors
Cubedo J,Padró T,Badimon Ldoi
10.1016/j.ijcard.2013.07.181subject
Has Abstractpub_date
2013-10-15 00:00:00pages
5196-204issue
6eissn
0167-5273issn
1874-1754pii
S0167-5273(13)01406-Xjournal_volume
168pub_type
杂志文章abstract:BACKGROUND:The platelet chemokine CXCL4 induces monocyte differentiation resulting in a macrophage phenotype called "M4", which co-expresses CD68, MMP7, and S100A8. We hypothesized that M4 macrophages are associated with plaque destabilization. METHODS:Atherosclerotic arteries were obtained from explanted hearts of pa...
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journal_title:International journal of cardiology
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journal_title:International journal of cardiology
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journal_title:International journal of cardiology
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journal_title:International journal of cardiology
pub_type: 杂志文章,多中心研究,随机对照试验
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journal_title:International journal of cardiology
pub_type: 杂志文章
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更新日期:2015-12-15 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.ijcard.2014.08.012
更新日期:2014-10-20 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章,多中心研究,随机对照试验
doi:10.1016/j.ijcard.2011.09.007
更新日期:2012-11-29 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
doi:10.1016/j.ijcard.2020.06.033
更新日期:2020-11-01 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
doi:10.1016/j.ijcard.2005.10.003
更新日期:2006-10-10 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
doi:10.1016/j.ijcard.2010.08.025
更新日期:2011-12-01 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
doi:10.1016/s0167-5273(97)02953-7
更新日期:1997-06-27 00:00:00
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更新日期:2017-05-15 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1016/j.ijcard.2007.02.030
更新日期:2008-04-25 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2001-06-01 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
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更新日期:2002-10-01 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
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更新日期:1996-09-01 00:00:00
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journal_title:International journal of cardiology
pub_type: 临床试验,杂志文章,多中心研究,随机对照试验
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更新日期:2005-05-11 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
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更新日期:2016-09-01 00:00:00
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journal_title:International journal of cardiology
pub_type: 杂志文章
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更新日期:2016-10-15 00:00:00