中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (3): 572-574.doi: 10.4103/1673-5374.320980

• 观点:视神经损伤修复保护与再生 • 上一篇    下一篇

S100 B注射引起的青光眼样损伤伴有小胶质细胞反应

  

  • 出版日期:2022-03-15 发布日期:2021-10-15

Glaucoma-like damage induced by S100B injection is accompanied by microglial response

Teresa Tsai, Stephanie C. Joachim*   

  1. Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany
  • Online:2022-03-15 Published:2021-10-15
  • Contact: Stephanie C. Joachim, MD, stephanie.joachim@rub.de.

摘要: Neural Regen Res:米诺环素结合降眼压是治疗青光眼的新策略
S100B是S100 蛋白家族的钙和锌结合蛋白,主要由星形胶质细胞表达,但也由视网膜和视神经中的小胶质细胞或少突胶质细胞表达。S100B 在信号转导、细胞分化、细胞运动调节、转录、蛋白质磷酸化、钙稳态和细胞凋亡等细胞过程中发挥作用。低浓度S100B具有神经保护作用并可促进神经突生长。另一方面,高浓度S100B 具有神经毒性特征。 
来自德国波鸿鲁尔大学大学的Stephanie C. Joachim团队认为,小胶质细胞可能是一种退行性因子,抑制小胶质细胞可保护神经元细胞免受青光眼样损伤。同时,在玻璃体内 S100B 模型中,引发线粒体和代谢功能障碍的进一步退行性因素发生了改变。由于低浓度的米诺环素可以保护视网膜神经节细胞和视神经神经丝,但不能完全阻止变性,因此其可能是青光眼等神经退行性眼病的一种辅助疗法。因此,将米诺环素结合降低眼压在青光眼治疗方向具有较大潜力。
文章在《中国神经再生研究(英文版)》杂志2022年 3月 3期发表。


https://orcid.org/0000-0001-7056-0829 (Stephanie C. Joachim)

Abstract: Glaucoma is currently the second leading cause of blindness worldwide. Due to aging societies the number of patients suffering from this disease will further increase in the next years. Unfortunately, glaucoma can remain asymptomatic until it is rather far progressed, hence about 10–50% of patients are unaware they suffer from this disease. Glaucoma is a progressive optic neuropathy associated with changes at the optic nerve head, gradual retinal ganglion cell (RGC) death, and visual field loss. High intraocular pressure (IOP) is the main risk factor, but the exact pathomechanism of glaucoma remains unexplained to date. In addition to mechanical damage due to increased IOP, which can injure axons and disrupt the ocular blood flow, numerous other factors have been recorded that contribute to the development of glaucoma. In recent years, the role of the immune system has come into focus as a possible contributor to glaucoma pathology. The involvement of immunological changes in glaucoma disease is based on the detection of altered antibody titer in serum samples of primary open-angle or normal-tension glaucoma patients and tear film samples of primary open-angle glaucoma patients. Affected patients showed antibodies against proteins such as heat shock protein (HSP)60, HSP27, or S100B (Grus et al., 2010; Bell et al., 2013).