Oxidative medicine and cellular longevity, 2016-01, Vol.2016 (2016), p.1-12
2016
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- Autor(en) / Beteiligte
- Titel
- An Abnormal Nitric Oxide Metabolism Contributes to Brain Oxidative Stress in the Mouse Model for the Fragile X Syndrome, a Possible Role in Intellectual Disability
- Ist Teil von
- Oxidative medicine and cellular longevity, 2016-01, Vol.2016 (2016), p.1-12
- Ort / Verlag
- Cairo, Egypt: Hindawi Publishing Corporation
- Erscheinungsjahr
- 2016
- Quelle
- Electronic Journals Library
- Beschreibungen/Notizen
- Background. Fragile X syndrome is the most common genetic cause of mental disability. Although many research has been performed, the mechanism underlying the pathogenesis is unclear and needs further investigation. Oxidative stress played major roles in the syndrome. The aim was to investigate the nitric oxide metabolism, protein nitration level, the expression of NOS isoforms, and furthermore the activation of the nuclear factor NF-κB-p65 subunit in different brain areas on the fragile X mouse model. Methods. This study involved adult male Fmr1-knockout and wild-type mice as controls. We detected nitric oxide metabolism and the activation of the nuclear factor NF-κBp65 subunit, comparing the mRNA expression and protein content of the three NOS isoforms in different brain areas. Results. Fmr1-KO mice showed an abnormal nitric oxide metabolism and increased levels of protein tyrosine nitrosylation. Besides that, nuclear factor NF-κB-p65 and inducible nitric oxide synthase appeared significantly increased in the Fmr1-knockout mice. mRNA and protein levels of the neuronal nitric oxide synthase appeared significantly decreased in the knockout mice. However, the epithelial nitric oxide synthase isoform displayed no significant changes. Conclusions. These data suggest the potential involvement of an abnormal nitric oxide metabolism in the pathogenesis of the fragile X syndrome.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1942-0900eISSN: 1942-0994DOI: 10.1155/2016/8548910Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4691629
- Format
- –
- Schlagworte
- Alzheimer's disease, Analysis, Animals, Blotting, Western, Brain, Brain - drug effects, Brain - metabolism, Brain - pathology, Brain research, Colleges & universities, Cytosol - metabolism, Disease Models, Animal, Fragile X Mental Retardation Protein - metabolism, Fragile X syndrome, Fragile X Syndrome - metabolism, Fragile X Syndrome - pathology, Gene expression, Grants, Hospitals, Intellectual disabilities, Intellectual Disability - metabolism, Intellectual Disability - pathology, Isoenzymes - metabolism, Kinases, Lipopolysaccharides - pharmacology, Metabolism, Mice, Knockout, Models, Biological, Nervous system, Neurons, Nitrates - metabolism, Nitration, Nitric oxide, Nitric Oxide - metabolism, Nitric Oxide Synthase Type I - metabolism, Nitric Oxide Synthase Type II - metabolism, Nitric Oxide Synthase Type III - metabolism, Nitrites - metabolism, Oxidative stress, Oxidative Stress - drug effects, Pathogenesis, Proteins, Real-Time Polymerase Chain Reaction, RNA, RNA, Messenger - genetics, RNA, Messenger - metabolism, Rodents, Tissue Culture Techniques, Transcription Factor RelA - metabolism, Transcription factors, Tyrosine, Tyrosine - analogs & derivatives, Tyrosine - metabolism