Rothermundt Matthias, Peters Marion, Prehn Jochen H M, Arolt Volker
Department of Psychiatry, University of Muenster, D-48149 Muenster, Germany.
Microsc Res Tech. 2003 Apr 15;60(6):614-32. doi: 10.1002/jemt.10303.
S100B is a calcium-binding peptide produced mainly by astrocytes that exert paracrine and autocrine effects on neurons and glia. Some knowledge has been acquired from in vitro and in vivo animal experiments to understand S100B's roles in cellular energy metabolism, cytoskeleton modification, cell proliferation, and differentiation. Also, insights have been gained regarding the interaction between S100B and the cerebral immune system, and the regulation of S100B activity through serotonergic transmission. Secreted glial S100B exerts trophic or toxic effects depending on its concentration. At nanomolar concentrations, S100B stimulates neurite outgrowth and enhances survival of neurons during development. In contrast, micromolar levels of extracellular S100B in vitro stimulate the expression of proinflammatory cytokines and induce apoptosis. In animal studies, changes in the cerebral concentration of S100B cause behavioral disturbances and cognitive deficits. In humans, increased S100B has been detected with various clinical conditions. Brain trauma and ischemia is associated with increased S100B concentrations, probably due to the destruction of astrocytes. In neurodegenerative, inflammatory and psychiatric diseases, increased S100B levels may be caused by secreted S100B or release from damaged astrocytes. This review summarizes published findings on S100B regarding human brain damage and neurodegeneration. Findings from in vitro and in vivo animal experiments relevant for human neurodegenerative diseases and brain damage are reviewed together with the results of studies on traumatic, ischemic, and inflammatory brain damage as well as neurodegenerative and psychiatric disorders. Methodological problems are discussed and perspectives for future research are outlined.
S100B是一种主要由星形胶质细胞产生的钙结合肽，对神经元和神经胶质细胞发挥旁分泌和自分泌作用。通过体外和体内动物实验，人们已获得了一些关于S100B在细胞能量代谢、细胞骨架修饰、细胞增殖和分化中作用的知识。此外，对于S100B与脑免疫系统之间的相互作用以及通过5-羟色胺能传递对S100B活性的调节也有了深入了解。分泌型神经胶质S100B根据其浓度发挥营养或毒性作用。在纳摩尔浓度下，S100B在发育过程中刺激神经突生长并提高神经元的存活率。相比之下，体外微摩尔水平的细胞外S100B刺激促炎细胞因子的表达并诱导细胞凋亡。在动物研究中，脑内S100B浓度的变化会导致行为障碍和认知缺陷。在人类中，在各种临床情况下都检测到S100B升高。脑外伤和缺血与S100B浓度升高有关，可能是由于星形胶质细胞的破坏。在神经退行性、炎症性和精神性疾病中，S100B水平升高可能是由分泌的S100B或受损星形胶质细胞释放所致。本综述总结了已发表的关于S100B与人脑损伤和神经退行性变相关的研究结果。综述了与人类神经退行性疾病和脑损伤相关的体外和体内动物实验结果，以及创伤性、缺血性和炎症性脑损伤以及神经退行性和精神性疾病的研究结果。讨论了方法学问题并概述了未来研究的前景。
