title: Variations in platelet proteins associated with ST-elevation myocardial infarction: novel clues on pathways underlying platelet activation in acute coronary syndromes.
abstract: 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).
  
  
  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.
authors.affiliation: Department of Pharmacology, Faculty of Pharmacy and Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
authors.forename: Andrés F
authors.initials: AF
authors.lastname: Parguiña
authors.forename: Lilian
authors.initials: L
authors.lastname: Grigorian-Shamagian
authors.forename: Rosa M
authors.initials: RM
authors.lastname: Agra
authors.forename: Diego
authors.initials: D
authors.lastname: López-Otero
authors.forename: Isaac
authors.initials: I
authors.lastname: Rosa
authors.forename: Jana
authors.initials: J
authors.lastname: Alonso
authors.forename: Elvis
authors.initials: E
authors.lastname: Teijeira-Fernández
authors.forename: José Ramón
authors.initials: JR
authors.lastname: González-Juanatey
authors.forename: Ángel
authors.initials: Á
authors.lastname: García
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000503:physiopathology*; D048868:Adaptor Proteins, Signal Transducing / Q000097:blood; D000368:Aged; D001792:Blood Platelets / Q000378:metabolism*; D001798:Blood Proteins / Q000378:metabolism*; D016022:Case-Control Studies; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D016023:Integrins / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology*; D009687:Nuclear Proteins / Q000097:blood; D015539:Platelet Activation / Q000502:physiology*; D010980:Platelet Membrane Glycoproteins / Q000378:metabolism; D011446:Prospective Studies; D017346:Protein Serine-Threonine Kinases / Q000097:blood; D040901:Proteomics; D015398:Signal Transduction / Q000502:physiology*; D015854:Up-Regulation; D019061:src-Family Kinases / Q000097:blood; D000099200:Scaffold Protein ILK
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D001798:Blood Proteins; D016023:Integrins; D009687:Nuclear Proteins; D010980:Platelet Membrane Glycoproteins; D017346:Protein Serine-Threonine Kinases; D019061:src-Family Kinases; D000099200:Scaffold Protein ILK; C082869:CRKL protein; C098341:platelet membrane glycoprotein VI