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Retinal ischemia triggers early microglia activation in the optic nerve followed by neurofilament degeneration.
Experimental Eye Research ( IF 3.0 ) Pub Date : 2020-07-06 , DOI: 10.1016/j.exer.2020.108133
Marina Palmhof 1 , Natalie Wagner 1 , Clarissa Nagel 1 , Nora Biert 1 , Gesa Stute 1 , H Burkhard Dick 1 , Stephanie C Joachim 1
Affiliation  

Retinal ischemia leads to an early severe damage of the retina and thus plays an important role in eye diseases such as angle-closure glaucoma or retinal vascular occlusion. In retinal diseases, there is common sense about the affection of the optic nerve by ischemic injury. However, the exact dynamic processes of this optic nerve degeneration are mainly unclear. In this study, retinal ischemia was induced in one eye of Brown-Norway rats by raising the intraocular pressure 60 min to 140 mmHg followed by natural reperfusion. Optic nerves were analyzed at six different points in time: 2, 6, 12, and 24 h as well as 3 and 7 days after ischemic injury. Cell infiltration and moreover signs of tissue demyelination and dissolution were noticed in optic nerves 7 days after ischemia (hematoxylin & eosin: p < 0.001, luxol fast blue: p = 0.04). Although microglial activation was verified already from 12 h on after ischemia (p = 0.030), the beginning of a structural degeneration of the neurofilament was seen at 3 days (p = 0.02). Interestingly, proliferative microglia were present later on (7 days: p = 0.017). At this point, the number of total microglia was also increased in ischemic nerves (p = 0.003). Concluding, our data indicate that not only retinal tissue is affected by an ischemia, the optic nerve also demonstrates progressive damage. Interestingly, a microglia activation was noted days before structural damage became visible.



中文翻译:

视网膜缺血会触发视神经中的小胶质细胞早期激活,然后引起神经丝变性。

视网膜缺血导致视网膜的早期严重损伤,因此在诸如闭角型青光眼或视网膜血管闭塞的眼部疾病中起重要作用。在视网膜疾病中,缺血性损伤对视神经的影响是常识。然而,这种视神经变性的确切动态过程主要尚不清楚。在这项研究中,通过将眼内压升高60分钟至140 mmHg,然后自然再灌注,在Brown-Norway大鼠的一只眼睛中诱发视网膜缺血。在六个不同的时间点对视神经进行了分析:2、6、12和24小时以及缺血性损伤后3和7天。在缺血后7天,在视神经中观察到细胞浸润以及组织脱髓鞘和溶解的迹象(苏木精和曙红:p <0.001,luxol固蓝:p = 0.04)。尽管从缺血后12小时起已经验证了小胶质细胞的激活(p = 0.030),但在3天时发现了神经丝结构性退化的开始(p = 0.02)。有趣的是,随后出现增生性小胶质细胞(7天:p = 0.017)。此时,缺血神经中的总小胶质细胞数量也增加了(p = 0.003)。最后,我们的数据表明,不仅视网膜组织受到缺血的影响,视神经还表现出进行性损伤。有趣的是,在可见结构破坏的前几天注意到小胶质细胞活化。017)。此时,缺血神经中的总小胶质细胞数量也增加了(p = 0.003)。最后,我们的数据表明,不仅视网膜组织受到缺血的影响,视神经还表现出进行性损伤。有趣的是,在可见结构破坏的前几天注意到小胶质细胞活化。017)。此时,缺血神经中的总小胶质细胞数量也增加了(p = 0.003)。最后,我们的数据表明,不仅视网膜组织受到缺血的影响,视神经还表现出进行性损伤。有趣的是,在可见结构破坏的前几天注意到小胶质细胞活化。

更新日期:2020-07-24
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