Tateishi Narito, Shimoda Taiji, Yada Nobumichi, Shinagawa Rika, Kagamiishi Yoshifumi
Minase Research Institute, Ono Pharmaceutical Co., Ltd., 3-1-1 Sakurai, Shimamoto, Mishima-gun, Osaka, 618-8585 Japan.
Nihon Shinkei Seishin Yakurigaku Zasshi. 2006 Feb;26(1):11-6.
The S100B is a Ca2+ binding proteins of EF-hand type and is produced primarily by astrocytes in the central nervous system. This protein has been implicated in the Ca2+-dependent regulation of a variety of intracellular functions such as protein phosphorylation, enzyme activities, cell proliferation and differentiation, dynamics of cytoskeleton constituents, structural organization of membranes, intracellular Ca2+ homeostasis, inflammation, and protection from oxidative cell damage. Recent studies suggest that released S100B exerts paracrine and autocrine effects on neurons and glia. On the other hand, elevations of S100B levels in blood or cerebrospinal fluid have been observed in patients with Alzheimer's disease, Down's syndrome, amyotrophic lateral sclerosis, multiple sclerosis, schizophrenia, depression, cerebral stroke and traumatic brain injury, and the levels have reached micromol/L-order at focal regions. It has been documented that the excessive S100B promotes the expression of inducible nitric oxide synthase or pro-inflammatory cytokines and exhibits detrimental effects on neurons. On studies using some animal models of the cerebral stroke or Alzheimer's disease, it is suggested that the excessive S100B produced by activated astrocytes precedes neurodegenerations. Authors discussed the relationship between neurological disorders and the S100B.
S100B是一种EF手型钙结合蛋白，主要由中枢神经系统中的星形胶质细胞产生。该蛋白与多种细胞内功能的钙依赖性调节有关，如蛋白质磷酸化、酶活性、细胞增殖与分化、细胞骨架成分的动力学、膜的结构组织、细胞内钙稳态、炎症以及免受氧化性细胞损伤。最近的研究表明，释放的S100B对神经元和神经胶质细胞具有旁分泌和自分泌作用。另一方面，在阿尔茨海默病、唐氏综合征、肌萎缩侧索硬化症、多发性硬化症、精神分裂症、抑郁症、脑卒中和创伤性脑损伤患者中，已观察到血液或脑脊液中S100B水平升高，且在局部区域已达到微摩尔/升水平。据记载，过量的S100B会促进诱导型一氧化氮合酶或促炎细胞因子的表达，并对神经元产生有害影响。在一些脑卒中和阿尔茨海默病动物模型的研究中，提示活化的星形胶质细胞产生的过量S100B先于神经退行性变出现。作者讨论了神经疾病与S100B之间的关系。
