Literature DB >> 21057855

Activation of mitogen activated protein kinases in post-infarcted patients.

Reza Akbarzadeh Najar1, Sayyed Mohammad Hossein Ghaderian, Akram Sadat Tabatabaei Panah.   

Abstract

Activation of mitogen-activated protein kinases (MAPKs) signaling cascade are important pathophysiologic regulators during the development of acute myocardial infarction (AMI). In present study, we designed to monitor the activity of these MAPKs in Iranian patients with AMI comparing with controls. The degree of activation (phosphorylation) of p38 kinase, p44/42 extracellular regulated kinase, and c-Jun N-terminal kinase (JNK1/2) and their corresponding activity levels were analyzed in 258 patients with AMI and 250 normal subjects. The expression of p38α mRNA was determined. These analysis were carried out immediately and 12 h after AMI. Activity of p38 and JNK1/2 MAPKs were significantly increased in patients with AMI than controls immediately after infarction. These activities were reduced during 12 h after AMI. However, there were no statistically differences in activation and activity of p44/42 in the patients and controls. The mRNA expression of p38α was increased in the patients comparing with controls. Results of this study indicate that these MAPKs signaling pathway might be activated by AMI which signal transduction involves kinase phosphorylation and play important roles in their activity. Elevated activity of p38 and JNK1/2 MAPKs suggests that they may potentially play significant roles in AMI.

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Year:  2011        PMID: 21057855     DOI: 10.1007/s11239-010-0526-9

Source DB:  PubMed          Journal:  J Thromb Thrombolysis        ISSN: 0929-5305            Impact factor:   2.300


  36 in total

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Journal:  Biochem Biophys Res Commun       Date:  1996-11-12       Impact factor: 3.575

2.  Pretreatment with adult progenitor cells improves recovery and decreases native myocardial proinflammatory signaling after ischemia.

Authors:  Meijing Wang; Ben M Tsai; Paul R Crisostomo; Daniel R Meldrum
Journal:  Shock       Date:  2006-05       Impact factor: 3.454

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Authors:  M Flesch; K B Margulies; H C Mochmann; D Engel; N Sivasubramanian; D L Mann
Journal:  Circulation       Date:  2001-11-06       Impact factor: 29.690

5.  Activation of mitogen-activated protein kinases in the non-ischemic myocardium of an acute myocardial infarction in rats.

Authors:  K Yoshida; M Yoshiyama; T Omura; Y Nakamura; S Kim; K Takeuchi; H Iwao; J Yoshikawa
Journal:  Jpn Circ J       Date:  2001-09

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Authors:  Y Wang; S Huang; V P Sah; J Ross; J H Brown; J Han; K R Chien
Journal:  J Biol Chem       Date:  1998-01-23       Impact factor: 5.157

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Journal:  Biochem J       Date:  2003-06-01       Impact factor: 3.857

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Journal:  Proc Natl Acad Sci U S A       Date:  1998-08-18       Impact factor: 11.205

9.  Targeted activation of c-Jun N-terminal kinase in vivo induces restrictive cardiomyopathy and conduction defects.

Authors:  Brian G Petrich; Benjamin C Eloff; Deborah L Lerner; Attila Kovacs; Jeffrey E Saffitz; David S Rosenbaum; Yibin Wang
Journal:  J Biol Chem       Date:  2004-01-23       Impact factor: 5.157

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Journal:  J Cell Biol       Date:  1998-07-27       Impact factor: 10.539

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  2 in total

1.  C-reactive protein (CRP) gene polymorphisms: implication in CRP plasma levels and susceptibility to acute myocardial infarction.

Authors:  Reza Akbarzadeh Najar; Sayyed Mohammad Hossein Ghaderian; Akram Sadat Tabatabaei Panah
Journal:  Mol Biol Rep       Date:  2011-07-01       Impact factor: 2.316

2.  Tumor necrosis factor-α: investigation of gene polymorphism and regulation of TACE-TNF-α system in patients with acute myocardial infarction.

Authors:  Sayyed Mohammad Hossein Ghaderian; Reza Akbarzadeh Najar; Akram Sadat Tabatabaei Panah
Journal:  Mol Biol Rep       Date:  2010-12-14       Impact factor: 2.316

  2 in total

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