ER stress upregulated PGE2/IFNγ-induced IL-6 expression and down-regulated iNOS expression in glial cells

被引：30

作者：

Hosoi, Toru ^{[1
]}

Honda, Miya ^{[1
]}

Oba, Tatsuya ^{[1
]}

Ozawa, Koichiro ^{[1
]}

机构：

[1] Hiroshima Univ, Grad Sch Biomed & Hlth Sci, Dept Pharmacotherapy, Minami Ku, Hiroshima 7348551, Japan

来源：

SCIENTIFIC REPORTS | 2013年 / 3卷

关键词：

ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; ALZHEIMERS-DISEASE; INDUCED APOPTOSIS; INTERLEUKIN-6; TRANSCRIPTION; RECEPTOR; TRANSLATION; INVOLVEMENT; ACTIVATION;

D O I：

10.1038/srep03388

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页数：6

共 39 条

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