S100B protein is released from rat neonatal neurons, astrocytes, and microglia by in vitro trauma and anti-S100 increases trauma-induced delayed neuronal injury and negates the protective effect of exogenous S100B on neurons
S100B protein is released from rat neonatal neurons, astrocytes, and microglia by in vitro trauma and anti-S100 increases trauma-induced delayed neuronal injury and negates the protective effect of exogenous S100B on neurons
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DOI：
10.1111/j.1471-4159.2007.04515.x
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发表时间：
2007-06-01
影响因子：
4.7
通讯作者：
Chen, Tao
中科院分区：
文献类型：
--
作者：
Ellis, Earl F.;Willoughby, Karen A.;Chen, Tao
S100 B蛋白存在于大脑中，已被用作脑损伤的标志物，并且具有神经营养性。使用一个良好的特点，在体外模型的脑细胞创伤，我们以前已经表明，应变损伤导致S100 B释放从新生大鼠神经元加神经胶质细胞培养物和外源性S100 B减少迟发性创伤后神经元损伤，即使在6或24小时创伤后。目前研究的目的是测量特定脑细胞类型的创伤后S100 B释放，并检查S100抗体对创伤后迟发性（48小时）神经元损伤的影响和外源性S100 B的保护作用。新生大鼠皮层细胞生长在一个可变形的弹性膜进行应变（拉伸）损伤所产生的50毫秒的位移的膜。用ELISA试剂盒测定S100 B。创伤从星形胶质细胞、小胶质细胞和神经元的纯培养物中释放S100 B。抗-S100将释放的S100 B减少到低于可检测的水平，增加创伤细胞中的迟发性神经元损伤，并且否定外源性S100 B对损伤细胞的保护作用。热变性抗S100没有加重损伤。这些研究为S100 B在神经元创伤后的保护作用提供了进一步的证据。
S100B protein is found in brain, has been used as a marker for brain injury and is neurotrophic. Using a well-characterized in vitro model of brain cell trauma, we have previously shown that strain injury causes S100B release from neonatal rat neuronal plus glial cultures and that exogenous S100B reduces delayed post-traumatic neuronal damage even when given at 6 or 24 h post-trauma. The purpose of the current studies was to measure post-traumatic S100B release by specific brain cell types and to examine the effect of an antibody to S100 on post-traumatic delayed (48 h) neuronal injury and the protective effect of exogenous S100B. Neonatal rat cortical cells grown on a deformable elastic membrane were subjected to a strain (stretch) injury produced by a 50 ms displacement of the membrane. S100B was measured with an ELISA kit. Trauma released S100B from pure cultures of astrocytes, microglia, and neurons. Anti-S100 reduced released S100B to below detectable levels, increased delayed neuronal injury in traumatized cells and negated the protective effect of exogenous S100B on injured cells. Heat denatured anti-S100 did not exacerbate injury. These studies provide further evidence for a protective role for S100B following neuronal trauma.