期刊
NEUROCHEMICAL RESEARCH
卷 38, 期 10, 页码 2216-2226出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-013-1130-0
关键词
SOC channels; Astrocyte activation; LPS
资金
- Natural Science Foundation of Guangdong Province [8151018201000039]
- Key Research Foundation of Guangzhou Education Bureau [2012C043]
- National Natural Science Foundation of China [81100986]
- Research Foundation of Guangzhou Education Bureau [10A154]
- Breeding Project of Guangdong Province [LYM11105]
The destruction of calcium homeostasis is an important factor leading to neurological diseases. Store-operated Ca2+ (SOC) channels are essential for Ca2+ homeostasis in many cell types. However, whether SOC channels are involved in astrocyte activation induced by lipopolysaccharide (LPS) still remains unknown. In this study, we used LPS as an exogenous stimulation to investigate the role of SOC channels in astrocyte activation. Using calcium imaging technology, we first found that SOC channels blockers, 1-[h-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole (SKF-96365) and 2-aminoethyldiphenyl borate (2-APB), inhibited LPS induced [Ca2+](i) increase, which prompted us to speculate that SOC channels may be involved in LPS induced astrocyte activation. Further experiments confirmed our speculation shown as SOC channels blockers inhibited LPS induced astrocyte activation characterized as cell proliferation by MTS and BrdU assay, raise in glial fibrillary acidic protein expression by immunofluorescence and Western Blot and secretion of interleukin 6 (IL-6) and interleukin 1 beta (IL-1 beta) by ELISA. So, our studies showed that SOC channels are involved in LPS-induced astrocyte activation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据