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.
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 cardiopathypatients. 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: Paula Vélez; Raymundo Ocaranza-Sánchez; Diego López-Otero; Lilian Grigorian-Shamagian; Isaac Rosa; Esteban Guitián; José María García-Acuña; José Ramón González-Juanatey; Ángel García Journal: Sci Rep Date: 2016-12-22 Impact factor: 4.379
Authors: Signe E Cremer; James L Catalfamo; Robert Goggs; Stefan E Seemann; Annemarie T Kristensen; Marjory B Brooks Journal: PLoS One Date: 2019-11-13 Impact factor: 3.240
Authors: Abhishek Joshi; Lukas E Schmidt; Sean A Burnap; Ruifang Lu; Melissa V Chan; Paul C Armstrong; Ferheen Baig; Clemens Gutmann; Peter Willeit; Peter Santer; Temo Barwari; Konstantinos Theofilatos; Stefan Kiechl; Johann Willeit; Timothy D Warner; Anthony Mathur; Manuel Mayr Journal: Arterioscler Thromb Vasc Biol Date: 2021-11-23 Impact factor: 8.311
Authors: Marta Lomnytska; Rui Pinto; Susanne Becker; Ulla Engström; Sonja Gustafsson; Christina Björklund; Markus Templin; Jan Bergstrand; Lei Xu; Jerker Widengren; Elisabeth Epstein; Bo Franzén; Gert Auer Journal: Biomark Res Date: 2018-01-12