Cerebrospinal fluid protein carbonylation identifies oxidative damage in autoimmune demyelination
dc.contributor.author | Irani, David N. | |
dc.date.accessioned | 2017-04-13T20:35:11Z | |
dc.date.available | 2018-05-04T20:56:58Z | en |
dc.date.issued | 2017-02 | |
dc.identifier.citation | Irani, David N. (2017). "Cerebrospinal fluid protein carbonylation identifies oxidative damage in autoimmune demyelination." Annals of Clinical and Translational Neurology 4(2): 145-150. | |
dc.identifier.issn | 2328-9503 | |
dc.identifier.issn | 2328-9503 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/136295 | |
dc.description.abstract | Oxidative damage occurs in multiple sclerosis, but is difficult to identify antemortem and remains an unknown contributor to disease progression. Carbonylation is a quantitative measure of protein oxidation. Cerebrospinal fluid samples from multiple sclerosis patients showed elevated carbonylated protein levels compared to controls. In experimental autoimmune encephalomyelitis, carbonylated protein levels in cerebrospinal fluid correlated tightly with those found in inflamed spinal cord tissues. Furthermore, concentrations in cerebrospinal fluid and spinal cord responded in parallel to an antioxidant intervention that also attenuated disease symptoms. These data suggest that carbonylated cerebrospinal fluid proteins could be a quantitative, sensitive, and disease‐relevant biomarker in multiple sclerosis. | |
dc.publisher | Wiley Periodicals, Inc. | |
dc.publisher | Saunders/Elsevier | |
dc.title | Cerebrospinal fluid protein carbonylation identifies oxidative damage in autoimmune demyelination | |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | |
dc.subject.hlbsecondlevel | Neurology and Neurosciences | |
dc.subject.hlbtoplevel | Health Sciences | |
dc.description.peerreviewed | Peer Reviewed | |
dc.description.bitstreamurl | https://deepblue.lib.umich.edu/bitstream/2027.42/136295/1/acn3379_am.pdf | |
dc.description.bitstreamurl | https://deepblue.lib.umich.edu/bitstream/2027.42/136295/2/acn3379.pdf | |
dc.identifier.doi | 10.1002/acn3.379 | |
dc.identifier.source | Annals of Clinical and Translational Neurology | |
dc.identifier.citedreference | Haider L, Fischer MT, Frischer JM, et al. Oxidative damage in multiple sclerosis. Brain 2011; 134: 1914 – 1924. | |
dc.identifier.citedreference | Fischer MT, Sharma R, Lim JL, et al. NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury. Brain 2012; 135: 886 – 899. | |
dc.identifier.citedreference | Bizzozero OA, DeJesus G, Callahan K, Pastuszyn A. Elevated protein carbonylation in the white matter and grey matter of patients with multiple sclerosis. J Neurosci Res 2005; 81: 687 – 695. | |
dc.identifier.citedreference | van Horssen J, Schreibelt G, Drexhage J, et al. Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression. Free Radic Biol Med 2008; 45: 1729 – 1737. | |
dc.identifier.citedreference | Fischer MT, Wimmer I, Hoftberger R, et al. Disease‐specific molecular events in cortical multiple sclerosis lesions. Brain 2013; 136: 1799 – 1815. | |
dc.identifier.citedreference | Kharel P, McDonough J, Basu S. Evidence of extensive RNA oxidation in normal appearing cortex of multiple sclerosis brain. Neurochem Int 2016; 92: 43 – 48. | |
dc.identifier.citedreference | Rogowska‐Wrzesinska A, Wojdyla K, Nedic O, et al. Analysis of protein carbonylation – pitfalls and promise in commonly used methods. Free Radic Res. 2014; 48: 1145 – 1162. | |
dc.identifier.citedreference | Korolainen MA, Pirttila T. Cerebrospinal fluid, serum and plasma protein oxidation in Alzheimer’s disease. Acta Neurol Scand 2009; 119: 32 – 38. | |
dc.identifier.citedreference | Rommer PS, Greilberger J, Salhofer‐Polanyi S, et al. Elevated levels of carbonyl proteins in cerebrospinal fluid of patients with neurodegenerative diseases. Tohoku J Exp Med 2014; 234: 313 – 317. | |
dc.identifier.citedreference | Blakely PK, Huber AK, Irani DN. Type‐1 angiotensin receptor signaling in central nervous system myeloid cells is pathogenic during fatal alphavirus encephalitis in mice. J Neuroinflammation 2016; 13: 196. doi: 10.1186/s12974‐016‐0683‐7. | |
dc.identifier.citedreference | Berlett BS, Stadtman ER. Protein oxidation in aging, disease and oxidative stress. J Biol Chem 1997; 272: 20313 – 20316. | |
dc.identifier.citedreference | Platten M, Youssef S, Hur EM, et al. Blocking angiotensin‐converting enzyme induces potent regulatory T cells and modulates Th1‐ and Th17‐mediated autoimmunity. Proc Natl Acad Sci USA 2009; 106: 14948 – 14953. | |
dc.identifier.citedreference | Stegbauer J, Lee DH, Seubert S, et al. Role of the renin‐angiotensin system in autoimmune inflammation of the central nervous system. Proc Natl Acad Sci USA 2009; 106: 14942 – 14947. | |
dc.identifier.citedreference | Lanz TV, Ding Z, Ho PP, et al. Angiotensin II sustains brain inflammation in mice via TGF‐beta. J. Clin. Invest. 2010; 120: 2782 – 2794. | |
dc.identifier.citedreference | Zheng J, Bizzozero OA. Reduced proteosomal activity contributes to the accumulation of carbonylated proteins in chronic experimental autoimmune encephalomyelitis. J Neurochem 2010; 115: 1556 – 1567. | |
dc.identifier.citedreference | Irani DN. Properties and composition of normal cerebrospinal fluid. In: Irani DN, ed. Cerebrospinal fluid in clinical practice. Philadelphia, PA: Saunders/Elsevier, 2009: 69 – 89. | |
dc.identifier.citedreference | Mahad DH, Trapp BD, Lassmann H. Pathological mechanisms in progressive multiple sclerosis. Lancet Neurol. 2015; 14: 183 – 193. | |
dc.identifier.citedreference | Lassmann H. Mechanisms of white matter damage in multiple sclerosis. Glia 2014; 62: 1816 – 1830. | |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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