Onodera Akira, Yayama Katsutoshi, Morosawa Hideto, Ishii Yukina, Tsutsumi Yasuo, Kawai Yuichi
Department of Pharmaceutical Sciences, Kobegakuin University, 1-1-3 Minatojima, Chuo-ku, Kobe 650-8586, Japan.
Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamada-oka, Suita, Osaka 565-0871, Japan.
Biochem Biophys Rep. 2017 Feb 4;9:330-334. doi: 10.1016/j.bbrep.2017.01.014. eCollection 2017 Mar.
Several studies have reported that amorphous nano-silica particles (nano-SPs) modulate calcium flux, although the mechanism remains incompletely understood. We thus analyzed the relationship between calcium flux and particle surface properties and determined the calcium flux route. Treatment of Balb/c 3T3 fibroblasts with nano-SPs with a diameter of 70 nm (nSP70) increased cytosolic calcium concentration, but that with SPs with a diameter of 300 or 1000 nm did not. Surface modification of nSP70 with a carboxy group also did not modulate calcium flux. Pretreatment with a general calcium entry blocker almost completely suppressed calcium flux by nSP70. Preconditioning by emptying the endoplasmic reticulum (ER) calcium stores slightly suppressed calcium flux by nSP70. These results indicate that nSP70 mainly modulates calcium flux across plasma membrane calcium channels, with subsequent activation of the ER calcium pump, and that the potential of calcium flux by nano-SPs is determined by the particle surface charge.
多项研究报告称，无定形纳米二氧化硅颗粒（纳米颗粒）可调节钙通量，但其机制仍未完全明确。因此，我们分析了钙通量与颗粒表面性质之间的关系，并确定了钙通量途径。用直径为70nm的纳米颗粒（nSP70）处理Balb/c 3T3成纤维细胞可增加细胞溶质钙浓度，但用直径为300或1000nm的颗粒处理则不会。用羧基对nSP70进行表面修饰也不会调节钙通量。用一般的钙内流阻滞剂预处理几乎完全抑制了nSP70引起的钙通量。通过排空内质网（ER）钙储存进行预处理可轻微抑制nSP70引起的钙通量。这些结果表明，nSP70主要通过质膜钙通道调节钙通量，随后激活ER钙泵，并且纳米颗粒引起钙通量的潜力由颗粒表面电荷决定。
