NF-κB Signaling in the Brain of Autistic Subjects
Autism is a neurodevelopmental disorder characterized by problems in communication, social skills, and repetitive behavior. Recent studies suggest that apoptotic and inflammatory mechanisms may contribute to the pathogenesis of this disorder. Nuclear factor-κB (NF-κB) is an important gene transcript...
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| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2011-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2011/785265 |
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| author | Mazhar Malik Zujaja Tauqeer Ashfaq M. Sheikh Guang Wen Amenah Nagori Kun Yang W. Ted Brown Xiaohong Li |
| author_facet | Mazhar Malik Zujaja Tauqeer Ashfaq M. Sheikh Guang Wen Amenah Nagori Kun Yang W. Ted Brown Xiaohong Li |
| author_sort | Mazhar Malik |
| collection | DOAJ |
| description | Autism is a neurodevelopmental disorder characterized by problems in communication, social skills, and repetitive behavior. Recent studies suggest that apoptotic and inflammatory mechanisms may contribute to the pathogenesis of this disorder. Nuclear factor-κB (NF-κB) is an important gene transcriptional factor involved in the mediation of inflammation and apoptosis. This study examined the activities of the NF-κB signaling pathway in the brain of autistic subjects and their age-matched controls. The NF-κB activation is also determined in the brain of BTBR mice, which is a promising animal model for study of pathogenic mechanisms responsible for autism. Our results showed that the level of IKKα kinase, which phosphorylates the inhibitory subunit IκBα, is significantly increased in the cerebellum of autistic subjects. However, the expression and phosphorylation of IκBα are not altered. In addition, our results demonstrated that the expression of NF-κB (p65), and the phosphorylation/activation of NF-κB (p65) at Ser536 are not significantly changed in the cerebellum and cortex of both autistic subjects and BTBR mice. Our findings suggest that the NF-κB signaling pathway is not disregulated in the brain of autistic subjects and thus may not be significantly involved in the processes of abnormal inflammatory responses suggested in autistic brain. |
| format | Article |
| id | doaj-art-fb778b8d8b1d49e9b19f481aefb0162d |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2011-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-fb778b8d8b1d49e9b19f481aefb0162d2025-02-03T05:58:51ZengWileyMediators of Inflammation0962-93511466-18612011-01-01201110.1155/2011/785265785265NF-κB Signaling in the Brain of Autistic SubjectsMazhar Malik0Zujaja Tauqeer1Ashfaq M. Sheikh2Guang Wen3Amenah Nagori4Kun Yang5W. Ted Brown6Xiaohong Li7Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USADepartment of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USADepartment of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USADepartment of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USADepartment of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USADepartment of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USADepartment of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USADepartment of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USAAutism is a neurodevelopmental disorder characterized by problems in communication, social skills, and repetitive behavior. Recent studies suggest that apoptotic and inflammatory mechanisms may contribute to the pathogenesis of this disorder. Nuclear factor-κB (NF-κB) is an important gene transcriptional factor involved in the mediation of inflammation and apoptosis. This study examined the activities of the NF-κB signaling pathway in the brain of autistic subjects and their age-matched controls. The NF-κB activation is also determined in the brain of BTBR mice, which is a promising animal model for study of pathogenic mechanisms responsible for autism. Our results showed that the level of IKKα kinase, which phosphorylates the inhibitory subunit IκBα, is significantly increased in the cerebellum of autistic subjects. However, the expression and phosphorylation of IκBα are not altered. In addition, our results demonstrated that the expression of NF-κB (p65), and the phosphorylation/activation of NF-κB (p65) at Ser536 are not significantly changed in the cerebellum and cortex of both autistic subjects and BTBR mice. Our findings suggest that the NF-κB signaling pathway is not disregulated in the brain of autistic subjects and thus may not be significantly involved in the processes of abnormal inflammatory responses suggested in autistic brain.http://dx.doi.org/10.1155/2011/785265 |
| spellingShingle | Mazhar Malik Zujaja Tauqeer Ashfaq M. Sheikh Guang Wen Amenah Nagori Kun Yang W. Ted Brown Xiaohong Li NF-κB Signaling in the Brain of Autistic Subjects Mediators of Inflammation |
| title | NF-κB Signaling in the Brain of Autistic Subjects |
| title_full | NF-κB Signaling in the Brain of Autistic Subjects |
| title_fullStr | NF-κB Signaling in the Brain of Autistic Subjects |
| title_full_unstemmed | NF-κB Signaling in the Brain of Autistic Subjects |
| title_short | NF-κB Signaling in the Brain of Autistic Subjects |
| title_sort | nf κb signaling in the brain of autistic subjects |
| url | http://dx.doi.org/10.1155/2011/785265 |
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