Jiang Yaqin, Zhang Canwei, Ma Jianli, Wang Luping, Gao Jing, Ren Jiantao, He Wei, Wang Sheng, Sheng Shuai, Huang Xudong
Department of Ophthalmology, Weifang Eye Hospital, Weifang, Shandong, People's Republic of China.
Department of Ophthalmology, University of Bonn, Bonn, Germany.
BMC Ophthalmol. 2019 Feb 4;19(1):43. doi: 10.1186/s12886-019-1058-5.
To investigate the expression of Matrix Metalloproteinases 2 and aquaporin-1 in corneoscleral junction and explore the mechanism of trabecular damageafter angle-closure.
Thirty New Zealand white rabbits were randomly assigned into 2 groups, theexperimental group (Group 1) including twenty five rabbits and the control group (Group 2) including 5 rabbits. The rabbits in the experimental group were used to establish angle-closure models, and the rabbits in the control group were not subjected to any operation. All the rabbits were followed by slit lamp microscopy, Tonopen tonometer, and anterior segment optical coherent tomography (AS-OCT). The expressions of metalloproteinase MMP-2, aquaporin-1, and tissue inhibitors of metalloproteinase-2 in corneoscleral junctionwere evaluatedin both groups byimmunofluorescence, quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA).
Slit-lamp examination showed that angle-closure model was successfully established in twenty rabbits. The extent of angle-closure was about 2 to 4 clock hours in all the rabbit models, but the intraocular pressure (IOP) of the rabbits distributed from 8.57 to 15.25 mmHg and no significant high IOP was found in the follow-up period. The AQP-1-positive cells mainly located in Schlemm's canal, the inner surface of trabecular meshwork (TM), and the surface of iris, which began to decline on 1 month after angle-closure. MMP2 staining was diffuse in trabecular meshwork and iris. Immunofluorescence signal of MMP2 was strong within 1 month after angle-closure, and subsequently became weak. qRT-PCR and ELISA showed that the expression of MMP-2 and TIMP-2 increased within 1 month after angle-closure and then declined gradually. The AQP-1 levels showed slightly declined on 1 month after angle-closure.
Altered levels of MMPs, TIMPs, and AQP-1 were found in the area of angle-closure, which may be involved in the damage of TM and Schlemm's canal after angle-closure.
探讨基质金属蛋白酶2和水通道蛋白-1在角巩膜缘的表达，以及闭角后小梁损伤的机制。
30只新西兰白兔随机分为2组，实验组（第1组）25只，对照组（第2组）5只。实验组兔用于建立闭角模型，对照组兔不进行任何手术。所有兔均通过裂隙灯显微镜、非接触眼压计和眼前段光学相干断层扫描（AS-OCT）进行随访。采用免疫荧光、定量逆转录聚合酶链反应（qRT-PCR）和酶联免疫吸附测定（ELISA）评估两组角巩膜缘中金属蛋白酶MMP-2、水通道蛋白-1和金属蛋白酶组织抑制剂-2的表达。
裂隙灯检查显示20只兔成功建立闭角模型。所有兔模型的闭角范围约为2至4个钟点，但兔眼压在8.57至15.25 mmHg之间分布，随访期间未发现明显高眼压。AQP-1阳性细胞主要位于施莱姆管、小梁网（TM）内表面和虹膜表面，在闭角后1个月开始下降。MMP2染色在小梁网和虹膜中呈弥漫性。MMP2免疫荧光信号在闭角后1个月内较强，随后变弱。qRT-PCR和ELISA显示，MMP-2和TIMP-2的表达在闭角后1个月内升高，然后逐渐下降。AQP-1水平在闭角后1个月略有下降。
在闭角区域发现MMPs、TIMPs和AQP-1水平改变，这可能与闭角后TM和施莱姆管的损伤有关。
