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基质金属蛋白酶9和金属蛋白酶组织抑制因子-1在绝对闭角型青光眼中视网膜和视神经的表达

Metalloproteinase 9 and TIMP-1 expression in retina and optic nerve in absolute angle closure glaucoma.

作者信息

Zalewska Renata, Reszeć Joanna, Kisielewski Wojciech, Mariak Zofia

机构信息

Department of Ophthalmology, Medical University of Bialystok, Bialystok, Poland.

Department of Medical Pathomorphology, Medical University of Bialystok, Bialystok, Poland.

出版信息

Adv Med Sci. 2016 Mar;61(1):6-10. doi: 10.1016/j.advms.2015.07.007. Epub 2015 Aug 9.

Abstract

PURPOSE

Glaucoma is one of the most important reason causes of the blindness, associated with retinal ganglion cells (RGC) death. This process is not fully understood, however apoptosis due to hypoxia is one of the most important processes leading to RGC death. Glaucomatous optic neuropathy is characterized by remodeling of the extracellular matrix due to metalloproteinase activation, which leads to loss of RGC and axons at the optic nerve head. The aim of the study was to evaluate metalloproteinase 9 (MMP-9) and tissue metalloproteinase inhibitor-1 (TIMP-1) expression in the retinal ganglion cells and optic nerve axons in 33 eyes with absolute primary glaucoma.

MATERIAL/METHODS: To evaluate MMP-9 and TIMP-1 expression primary polyclonal goat antibodies against MMP-9 and TIMP-1 were used. The control group was composed of 8 cases of eyes enucleated and fixed in the first day after trauma.

RESULTS

MMP-9 expression was observed in retinal ganglion cells and in the inner nuclear layer of the retina in all the examined cases. In 28 out of 33 glaucomatous eyes, MMP-9 expression was observed in the proliferating glial cells surrounding the optic nerve axons. TIMP-1 expression was observed in 10 out of 33 glaucomatous eyes, only in retinal ganglion cells. None of the examined injured eyes showed MMP-9 and TIMP-1 expression.

CONCLUSIONS

MMP-9 activation rather than TIMP-1 may by associated with the pathomechanism of retinal ganglion cell and optic nerve damage in absolute glaucoma.

摘要

目的

青光眼是导致失明的最重要原因之一,与视网膜神经节细胞(RGC)死亡相关。然而,这一过程尚未完全明确,不过缺氧诱导的细胞凋亡是导致RGC死亡的最重要过程之一。青光眼性视神经病变的特征是由于金属蛋白酶激活导致细胞外基质重塑,进而引起视神经乳头处RGC和轴突的丧失。本研究的目的是评估33只绝对期原发性青光眼患眼中视网膜神经节细胞和视神经轴突中金属蛋白酶9(MMP - 9)和组织金属蛋白酶抑制剂 - 1(TIMP - 1)的表达情况。

材料/方法:为评估MMP - 9和TIMP - 1的表达,使用了抗MMP - 9和TIMP - 1的原发性多克隆山羊抗体。对照组由8例外伤后第一天摘除并固定的眼球组成。

结果

在所有检查病例中,均在视网膜神经节细胞和视网膜内核层观察到MMP - 9表达。在33只青光眼眼中,有28只在围绕视神经轴突的增殖性胶质细胞中观察到MMP - 9表达。在33只青光眼眼中,有10只仅在视网膜神经节细胞中观察到TIMP - 1表达。所有检查的受伤眼均未显示MMP - 9和TIMP - 1表达。

结论

在绝对期青光眼中,MMP - 9的激活而非TIMP - 1可能与视网膜神经节细胞和视神经损伤的发病机制相关。

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