dc.contributor.author | Meng, Fanjun | eng |
dc.contributor.author | Liu, Siqi | eng |
dc.contributor.author | Gu, Zezong | eng |
dc.contributor.corporatename | University of Missouri (System) | eng |
dc.contributor.meetingname | Missouri Life Sciences Summit (2010: University of Missouri--Kansas City) | eng |
dc.date.issued | 2010-02 | eng |
dc.description | Neuroscience - Vision & Functional Brain Imaging Poster Session | eng |
dc.description.abstract | A convergent feature for most aging-related neurological diseases, such as Parkinson's Disease (PD), is excessive generation of free radicals - reactive nitrogen and oxygen species, which can contribute to neuronal cell death and link to the disease pathogenesis. Free radical nitric oxide (NO) is a signaling molecule involving in the regulation of a wide range of cellular functions from development to disease. Emerging evidence suggests that nitrosative stress due to NO over-production induces post-translational modifications of protein cysteine and modulates protein enzymatic activity in cells. S-Nitrosylation, the covalent adduction of NO to specific protein cysteine thiol, is considered as a predominant, redox-based prototypical mechanism for cell signaling. Previously, endogenous protein S-nitrosylation was detected by the biotin switch assay. Taking the advantages of both biotin switch assay and differential in-gel electrophoresis (DIGE), we developed a gel-based proteomics method, named as NitroDIGE, to globally and quantitatively investigate protein S-nitrosylation. Using this method, we identified a subset of S-nitrosylated proteins from both in vitro and in vivo models of Parkinsonism including pesticide rotenone-induced PD-relevant insults in SH-SY5Y cells. Moreover, we determined whether protein S-nitrosylation in cellular PD models could be modulated by different botanical phenolic compounds, including epigallocatechin gallate (EGCG) from green tea, and apocynin from Picrorhiza kurrooa, a herbal plant grown in the Himalayan. The NitroDIGE results demonstrated that the treatment of botanical compounds could reduce excessive S-nitrosylated proteins in SH-SY5Y cells exposed to rotenone, indicating that these botanical phenolics could serve as effective NO scavengers to attenuate nitrosative stress and PD-relevant insults. | eng |
dc.identifier.uri | http://hdl.handle.net/10355/5615 | eng |
dc.language | English | eng |
dc.relation.ispartof | Abstracts (Missouri Regional Life Sciences Summit 2010) | eng |
dc.relation.ispartofcommunity | University of Missouri System. Missouri Summits. Missouri Regional Life Sciences Summit 2010 | eng |
dc.subject | neurological diseases | eng |
dc.subject | neuronal cell death | eng |
dc.subject | nitric oxide | eng |
dc.subject | botanical phenolic compounds | eng |
dc.subject.lcsh | Neurons | eng |
dc.subject.lcsh | Apoptosis | eng |
dc.subject.lcsh | Nitric oxide | eng |
dc.subject.lcsh | Phenols | eng |
dc.title | Quantitative Profiling of S-Nitrosylated Proteins in Parkinson's Disease Paradigms for the Effects of Botanical Phenolics [abstract] | eng |
dc.type | Abstract | eng |