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吸入钒会在小鼠模型中引发视网膜穆勒胶质细胞(MGC)改变。

Vanadium inhalation induces retinal Müller glial cell (MGC) alterations in a murine model.

作者信息

Cervantes-Yépez Silvana, López-Zepeda Lorena Sofía, Fortoul Teresa I

机构信息

a Departamento de Biología Celular y Tisular, Facultad de Medicina , Universidad Nacional Autónoma de México (UNAM) , México City , CP , México.

出版信息

Cutan Ocul Toxicol. 2018 Jun;37(2):200-206. doi: 10.1080/15569527.2017.1392560. Epub 2017 Dec 11.

DOI:10.1080/15569527.2017.1392560
PMID:29157004
Abstract

BACKGROUND

Vanadium (V) is a transition metal adhered to suspended particles. Previous studies demonstrated that V inhalation causes oxidative stress in the ependymal epithelium, the choroid plexus on brain lateral ventricles and in the retina. Inhaled-V reaches the eye´s retina through the systemic circulation; however, its effect on the retina has not been widely studied. The Müller glial cell provides support and structure to the retina, facilitates synapses and regulates the microenvironment and neuronal metabolism. Hence, it is of great interest to study the effect of V exposure on the expression and localization of specific biomarkers on this cell.

METHODS

Male CD-1 mice were exposed to V inhalation 1 h/twice/week for 4 and 8-Wk. Expression changes in the retina of Glial fibrillary acidic protein, highly expressed in Müller glial cell when retina is damaged, and Glutamine synthetase, important in preventing excitotoxicity in the retina, were analysed by immunohistochemistry.

RESULTS

Glial fibrillary acidic protein expression increased at 4-Wk of V inhalation compared to the control and decreased at 8-Wk of exposure. A time-dependent gradual reduction in glutamine synthetase expression was observed.

CONCLUSION

Changes in glial fibrillary acidic protein expression induced by V suggest retinal damage, whereas glutamine synthetase gradual reduction might indicate that photoreceptors, which produce most of the glutamine synthetase substrate in the retina, are degenerating, probably as a consequence of the oxidative stress induced by V.

摘要

背景

钒(V)是一种附着于悬浮颗粒的过渡金属。先前的研究表明,吸入钒会在室管膜上皮、脑侧脑室脉络丛和视网膜中引起氧化应激。吸入的钒通过体循环到达眼睛的视网膜;然而,其对视网膜的影响尚未得到广泛研究。米勒胶质细胞为视网膜提供支持和结构,促进突触形成并调节微环境和神经元代谢。因此,研究钒暴露对该细胞上特定生物标志物的表达和定位的影响具有重要意义。

方法

雄性CD-1小鼠每周两次、每次1小时吸入钒,持续4周和8周。通过免疫组织化学分析胶质纤维酸性蛋白(在视网膜受损时在米勒胶质细胞中高表达)和谷氨酰胺合成酶(对预防视网膜兴奋性毒性很重要)在视网膜中的表达变化。

结果

与对照组相比,吸入钒4周时胶质纤维酸性蛋白表达增加,暴露8周时下降。观察到谷氨酰胺合成酶表达呈时间依赖性逐渐降低。

结论

钒诱导的胶质纤维酸性蛋白表达变化提示视网膜损伤,而谷氨酰胺合成酶的逐渐降低可能表明视网膜中产生大部分谷氨酰胺合成酶底物的光感受器正在退化,这可能是钒诱导的氧化应激的结果。

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