Expression of calbindin-D28k in C6 glial cells stabilizes intracellular calcium levels and protects against apoptosis induced by calcium ionophore and amyloid β-peptide

摘要: The calcium binding protein, calbindin-D28k is normally present in neurons. Recently we reported that brain injury and tumor necrosis factors (TNFs) induce astrocytes. TNF-treated calbindin expressing astrocytes were resistant to acidosis ionophore toxicity, suggesting may have a cytoprotective role the injured (M.P. Mattson, B. Cheng, S.A. Baldwin, V.L. Smith-Swintosky, J. Keller, Geddes, Scheff, J.W., Christakos, S., Brain astrocytes: evidence for response, Neurosci. Res., 42 (1995) 257). In order obtain direct of calbindin, using eukaryotic expression vector pREP4, rat was stably expressed C6 astocytoma glial cells. Cytotoxicity response or amyloid beta-peptide (which accumulates Alzheimer's disease has been be neurotoxic) measured by MTT reduction transfected cells clones. Stably resulted increased cell survival presence (1-10 microM) (10-100 microM). addition, mediated rise intracellular significantly attenuated Apoptotic death detected Hoechst method treated with beta-amyloid (34-36% apoptotic cells/culture). number nuclei similarly clones (10-13% cells/culture; p<0.01). Our results support involvement fluxes apoptosis suggest calbindin-D28k, buffering calcium, can suppress susceptible central nervous system.