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Neurochem Res ; 38(10): 2216-26, 2013 Oct.
Article in English | MEDLINE | ID: mdl-23974726

ABSTRACT

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 1ß (IL-1ß) by ELISA. So, our studies showed that SOC channels are involved in LPS-induced astrocyte activation.


Subject(s)
Astrocytes/physiology , Calcium Channel Blockers/pharmacology , Calcium Channels/physiology , Imidazoles/pharmacology , Lipopolysaccharides/pharmacology , Animals , Astrocytes/drug effects , Boron Compounds/pharmacology , Calcium Channels/drug effects , Calcium Signaling/drug effects , Cell Proliferation/drug effects , Cells, Cultured , Female , Glial Fibrillary Acidic Protein/biosynthesis , Interleukin-1beta/metabolism , Interleukin-6/metabolism , Male , Rats , Rats, Wistar
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