Journal
SCIENTIFIC REPORTS
Volume 3, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep03388
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Funding
- Ministry of Education, Culture, Sports, Science, and Technology, Japan
- Takeda Science Foundation
- Tokyo Biochemical Research Foundation
- Suzuken Memorial Foundation
- Nakajima Foundation
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The disruption of endoplasmic reticulum (ER) function can lead to neurodegenerative disorders, in which inflammation has also been implicated. We investigated the possible correlation between ER stress and immune function using glial cells. We demonstrated that ER stress synergistically enhanced prostaglandin (PG) E-2 + interferon (IFN) gamma-induced interleukin (IL)-6 production. This effect was mediated through cAMP. Immune-activated glial cells produced inducible nitric oxide synthase (iNOS). Interestingly, ER stress inhibited PGE(2) + IFN gamma-induced iNOS expression. Similar results were obtained when cells were treated with dbcAMP + IFN gamma. Thus, cAMP has a dual effect on immune reactions; cAMP up-regulated IL-6 expression, but down-regulated iNOS expression under ER stress. Therefore, our results suggest a link between ER stress and immune reactions in neurodegenerative diseases.
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