Biomarkers for ischemic stroke subtypes: A protein-protein interaction analysis |
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| Affiliation: | 1. Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI 48202, USA;2. Department of Computer Science, Wayne State University College of Engineering, Detroit, MI, USA;3. SJTU-Yale Joint Centre for Biostatistics, Shanghai Jiao Tong University, Shanghai, China;4. Department of Bioinformatics and Biostatistics, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China;5. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI 48201, USA;6. Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI 48109, USA;7. Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI 48825, USA;8. Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48201, USA;9. School of Mathematical Sciences, Shanghai Jiao Tong University, Shanghai, China;1. Laboratoire de Chimie des Matériaux, Faculté des Sciences de Bizerte, 7021 Zarzouna, Université de Carthage, Tunisia;2. Laboratoire des substances bio-actives, Faculté des Sciences de Bizerte 7021 Zarzouna, Université de Carthage, Tunisia |
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| Abstract: | According to the Trial of Org 10172 in Acute Stroke Treatment, ischemic stroke is classified into five subtypes. However, the predictive biomarkers of ischemic stroke subtypes are still largely unknown. The utmost objective of this study is to map, construct and analyze protein-protein interaction (PPI) networks for all subtypes of ischemic stroke, and to suggest the predominant biological pathways for each subtypes. Through 6285 protein data retrieved from PolySearch2 and STRING database, the first PPI networks for all subtypes of ischemic stroke were constructed. Notably, F2 and PLG were identified as the critical proteins for large artery atherosclerosis (LAA), lacunar, cardioembolic, stroke of other determined etiology (SOE) and stroke of undetermined etiology (SUE). Gene ontology and DAVID analysis revealed that GO:0030193 regulation of blood coagulation and GO:0051917 regulation of fibrinolysis were the important functional clusters for all the subtypes. In addition, inflammatory pathway was the key etiology for LAA and lacunar, while FOS and JAK2/STAT3 signaling pathways might contribute to cardioembolic stroke. Due to many risk factors associated with SOE and SUE, the precise etiology for these two subtypes remained to be concluded. |
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| Keywords: | Ischemic stroke subtypes Protein-protein interaction LAA Lacunar Cardioembolic SOE SUE Prothrombin (F2) Plasminogen |
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