dc.creator | Koo, Sue Jie | |
dc.creator | Spratt, Heidi M. | |
dc.creator | Soman, Kizhake V. | |
dc.creator | Stafford, Susan | |
dc.creator | Gupta, Shivali | |
dc.creator | Petersen, John R. | |
dc.creator | Zago, María Paola | |
dc.creator | Kuyumcu Martinez, Muge N. | |
dc.creator | Brasier, Allan R. | |
dc.creator | Wiktorowicz, John E. | |
dc.creator | Garg, Nisha Jain | |
dc.date.accessioned | 2018-02-27T18:32:09Z | |
dc.date.available | 2018-02-27T18:32:09Z | |
dc.date.created | 2018-02-27T18:32:09Z | |
dc.date.issued | 2016 | |
dc.identifier | Koo, Sue Jie; Spratt, Heidi M.; Soman, Kizhake V.; Stafford, Susan; Gupta, Shivali; et al.; S-Nitrosylation Proteome Profile of Peripheral Blood Mononuclear Cells in Human Heart Failure; Hindawi Publishing Corporation; International Journal of Proteomics; 2016; 2016; 1-19; 1384523 | |
dc.identifier | 2090-2174 | |
dc.identifier | http://hdl.handle.net/11336/37293 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.description.abstract | Nitric oxide (NO) protects the heart against ischemic injury; however, NO- and superoxide-dependent S-nitrosylation (S-NO) of cysteines can affect function of target proteins and play a role in disease outcome. We employed 2D-GE with thiol-labeling FL-maleimide dye and MALDI-TOF MS/MS to capture the quantitative changes in abundance and S-NO proteome of HF patients (versus healthy controls, n = 30/group). We identified 93 differentially abundant (59-increased/34-decreased) and 111 S-NO-modified (63-increased/48-decreased) protein spots, respectively, in HF subjects (versus controls, fold-change | ≥1.5|, p ≤ 0.05). Ingenuity pathway analysis of proteome datasets suggested that the pathways involved in phagocytes´ migration, free radical production, and cell death were activated and fatty acid metabolism was decreased in HF subjects. Multivariate adaptive regression splines modeling of datasets identified a panel of proteins that will provide >90% prediction success in classifying HF subjects. Proteomic profiling identified ATP-synthase, thrombospondin-1 (THBS1), and vinculin (VCL) as top differentially abundant and S-NO-modified proteins, and these proteins were verified by Western blotting and ELISA in different set of HF subjects. We conclude that differential abundance and S-NO modification of proteins serve as a mechanism in regulating cell viability and free radical production, and THBS1 and VCL evaluation will potentially be useful in the prediction of heart failure. | |
dc.language | eng | |
dc.publisher | Hindawi Publishing Corporation | |
dc.relation | info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1155/2016/1384523 | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/https://www.hindawi.com/journals/ijpro/2016/1384523/ | |
dc.rights | https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | S-NITROSYLATION | |
dc.subject | PROTEOMIC PROFILING | |
dc.subject | HEART FAILURE | |
dc.title | S-Nitrosylation Proteome Profile of Peripheral Blood Mononuclear Cells in Human Heart Failure | |
dc.type | info:eu-repo/semantics/article | |
dc.type | info:ar-repo/semantics/artículo | |
dc.type | info:eu-repo/semantics/publishedVersion | |