ER stress-mediated regulation of immune function under glucose-deprived condition in glial cells: Up- and down-regulation of PGE2+ IFNγ-induced IL-6 and iNOS expressions
書誌事項
- 公開日
- 2013-11
- 資源種別
- journal article
- 権利情報
-
- https://www.elsevier.com/tdm/userlicense/1.0/
- https://www.elsevier.com/legal/tdmrep-license
- DOI
-
- 10.1016/j.bbrc.2013.10.109
- 公開者
- Elsevier BV
この論文をさがす
説明
Glucose metabolism plays central role in maintaining brain function. Under ischemic condition, where glucose levels were reduced, glial cells induce pro-inflammatory cytokine production. In the present study, we found prostaglandin (PG) E2+interferon (IFN) γ-induced interleukin (IL)-6 production was enhanced under glucose-deprived condition in the primary cultured glial cells. On the other hand, to our surprise, we found that PGE2+IFNγ-induced iNOS expression was attenuated under glucose-deprived condition. These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition. By activating theses responses glial cells may protect neurons because we observed increased neuronal cell viability in the immune-activated glial cell conditioned medium. Overall, our results suggest a link between ER stress and immune reactions under glucose-deprived condition in the glial cells.
収録刊行物
-
- Biochemical and Biophysical Research Communications
-
Biochemical and Biophysical Research Communications 441 (2), 525-528, 2013-11
Elsevier BV
