Variations in platelet proteins associated with ST-elevation myocardial infarction: novel clues on pathways underlying platelet activation in acute coronary syndromes.

نویسندگان

  • Andrés F Parguiña
  • Lilian Grigorian-Shamagian
  • Rosa M Agra
  • Diego López-Otero
  • Isaac Rosa
  • Jana Alonso
  • Elvis Teijeira-Fernández
  • José Ramón González-Juanatey
  • Ángel García
چکیده

OBJECTIVE Our aim in this study was to provide novel information on the molecular mechanisms playing a major role in the unwanted platelet activation associated with ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS We compared the platelet proteome of 11 STEMI patients to a matched control group of 15 stable chronic ischemic cardiopathy patients. In addition, we did a prospective study to follow the STEMI patients over time. Proteins were separated by high-resolution 2D gel electrophoresis, identified by mass spectrometry, and validated by Western blotting. Platelets from STEMI patients on admission displayed 56 protein spot differences (corresponding to 42 unique genes) compared with the control group. The number of differences decreased with time during the patients' follow-up. Interestingly, the adapter protein CrkL and the active form of Src (phosphorylated in Tyr418) were found to be upregulated in platelets from STEMI patients. Major signaling pathways related to the proteins identified include integrin, integrin-linked kinase, and glycoprotein VI (GPVI) signaling. Interestingly, a study on an independent cohort of patients showed a higher degree of activation of GPVI signaling in STEMI patients. CONCLUSIONS CrkL, the active form of Src, and GPVI signaling are upregulated in platelets from STEMI patients.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

No-Reflow Phenomenon in Patients with ST-Elevation Acute Myocardial Infarction, Treated with Primary Percutaneous Coronary Intervention: A Study of Predictive Factors

  Introduction: No-reflow phenomenon in coronary vessels, manifested in some patients with reperfused acute myocardial infarction (MI), is associated with poor clinical and functional outcomes. Therefore, evaluation of predisposing risk factors can be helpful in risk assessment and identification of patients at higher risk. Herein, we aimed to study the predictive factors for the development of...

متن کامل

Mean platelet volume in ST elevation and non-ST elevation myocardial infarction

Platelet activation is thought to play a key pathogenetic mechanism in acute coronary syndromes. We investigated the mean platelet volume and platelet count in patients with both ST elevation myocardial infarction and non-ST elevation myocardial infarction. Fifty two patients with non-ST elevation myocardial infarction and 56 patients with ST elevation myocardial infarction were enrolled in the...

متن کامل

Platelet-To-Lymphocyte Ratio as a Predictor of No-Reflow after Primary Percutaneous Coronary Intervention in Patients with ST Elevation Myocardial Infarction: A Systematic Review and Meta-Analysis

Introduction: No-reflow increases the complications and mortality rate of primary percutaneous coronary intervention (PCI). Therefore, it is important to identify patients at a higher risk of developing no-reflow. This study aimed to systematically review the prognostic value of the platelet-to-lymphocyte ratio (PLR) to predict no-reflow. Materials and Methods:</s...

متن کامل

Inhibitors of platelet adhesion.

Platelet aggregation, in fundamental terms, is considered a biological end point that contributes to the occurrence of clinical events among patients with advanced atherosclerotic coronary artery disease. Acute coronary syndrome, including non–ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI), accounts for upward of 733 000 hospital admissions yearly in ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Arteriosclerosis, thrombosis, and vascular biology

دوره 31 12  شماره 

صفحات  -

تاریخ انتشار 2011