Alpha-synuclein deficiency leads to increased glyoxalase I expression and glycation stress
| العنوان: | Alpha-synuclein deficiency leads to increased glyoxalase I expression and glycation stress |
|---|---|
| المؤلفون: | Georg Auburger, Michael Bonin, Suzana Gispert, Paul J. Thornalley, Naila Rabbani, Michael Walter, Alexander Kurz |
| المصدر: | Cellular and Molecular Life Sciences |
| بيانات النشر: | SP Birkhäuser Verlag Basel, 2010. |
| سنة النشر: | 2010 |
| مصطلحات موضوعية: | Glycation End Products, Advanced, Male, medicine.medical_specialty, Glycosylation, Carbohydrate metabolism, Motor Activity, Polymerase Chain Reaction, Alpha-synuclein deficiency, Transcriptome, chemistry.chemical_compound, Lactoylglutathione lyase, Cellular and Molecular Neuroscience, Mice, Glycation, Internal medicine, medicine, Animals, ddc:610, Molecular Biology, Alpha-synuclein, Regulation of gene expression, Pharmacology, Mice, Knockout, Glucose metabolism, biology, Microarray analysis techniques, Gene Expression Profiling, Methylglyoxal, Lactoylglutathione Lyase, Advanced glycation endproducts, Brain, Cell Biology, Glyoxalase I, QP, Transcriptome microarray, Endocrinology, Glucose, chemistry, Biochemistry, Gene Expression Regulation, biology.protein, alpha-Synuclein, Molecular Medicine, Research Article |
| الوصف: | The presynaptic protein alpha-synuclein has received much attention because its gain-of-function is associated with Parkinson’s disease. However, its physiological function is still poorly understood. We studied brain regions of knock-out mice at different ages with regard to consistent upregulations of the transcriptome and focused on glyoxalase I (GLO1). The microarray data were confirmed in qPCR, immunoblot, enzyme activity, and behavior analyses. GLO1 induction is a known protective cellular response to glucose stress, representing efforts to decrease toxic levels of methylglyoxal (MG), glyoxal and advanced glycation endproducts (AGEs). Mass spectrometry quantification demonstrated a ubiquitous increase in MG and fructosyl-lysine as consequences of glucose toxicity, and consistent enhancement of certain AGEs. Thus, GLO1 induction in KO brain seems insufficient to prevent AGE formation. In conclusion, the data demonstrate GLO1 expression and glycation damage to be induced by alpha-synuclein ablation. We propose that wild-type alpha-synuclein modulates brain glucose metabolism. |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 1420-9071 1420-682X |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::24af306a2f51487959bdd77c9228055cTest http://europepmc.org/articles/PMC3029823Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....24af306a2f51487959bdd77c9228055c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14209071 1420682X |
|---|