Hosoi Toru, Saito Atsushi, Kume Ayaka, Okuma Yasunobu, Nomura Yasuyuki, Ozawa Koichiro
Department of Pharmacotherapy, Graduate School of Biomedical Sciences, Hiroshima University, Kasumi 1-2-3, Hiroshima 734-8553, Japan.
Eur J Pharmacol. 2008 Oct 10;594(1-3):44-8. doi: 10.1016/j.ejphar.2008.07.034. Epub 2008 Jul 30.
The disruption of endoplasmic reticulum function leads to an accumulation of unfolded proteins, which results in endoplasmic reticulum stress. In the present study, we investigated the effect of vanadate on such stress. Endoplasmic reticulum stress increased glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) expressions in glial cell cultures. We found that vanadate inhibited the endoplasmic reticulum stress-induced increase in GRP78 and CHOP expressions at both mRNA and protein levels. Thus, these results suggest that vanadate modulates endoplasmic reticulum stress responses and that novel vanadate-responsive protein(s) might be involved in these processes.
内质网功能紊乱会导致未折叠蛋白的积累，进而引发内质网应激。在本研究中，我们调查了钒酸盐对这种应激的影响。内质网应激会增加神经胶质细胞培养物中葡萄糖调节蛋白78（GRP78）和CCAAT/增强子结合蛋白同源蛋白（CHOP）的表达。我们发现，钒酸盐在mRNA和蛋白质水平上均抑制了内质网应激诱导的GRP78和CHOP表达的增加。因此，这些结果表明钒酸盐可调节内质网应激反应，并且新的钒酸盐反应蛋白可能参与了这些过程。
