Store-Operated Ca2+ Channels Blockers Inhibit Lipopolysaccharide Induced Astrocyte Activation
The destruction of calcium homeostasis is an important factor leading to neurological diseases. Store-operated Ca 2+ (SOC) channels are essential for Ca 2+ homeostasis in many cell types. However, whether SOC channels are involved in astrocyte activation induced by lipopolysaccharide (LPS) still rem...
Saved in:
Published in | Neurochemical research Vol. 38; no. 10; pp. 2216 - 2226 |
---|---|
Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Boston
Springer US
01.10.2013
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | The destruction of calcium homeostasis is an important factor leading to neurological diseases. Store-operated Ca
2+
(SOC) channels are essential for Ca
2+
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 [Ca
2+
]
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 1β (IL-1β) by ELISA. So, our studies showed that SOC channels are involved in LPS-induced astrocyte activation. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0364-3190 1573-6903 |
DOI: | 10.1007/s11064-013-1130-0 |