增殖性玻璃体视网膜病变中的明胶酶B

Gelatinase B in proliferative vitreoretinal disorders.

作者信息

Abu El-Asrar A M, Dralands L, Veckeneer M, Geboes K, Missotten L, Van Aelst I, Opdenakker G

机构信息

Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.

出版信息

Am J Ophthalmol. 1998 Jun;125(6):844-51. doi: 10.1016/s0002-9394(98)00041-5.

DOI:10.1016/s0002-9394(98)00041-5

PMID:9645722

Abstract

PURPOSE

To investigate whether gelatinases A and B are involved in the pathogenesis of proliferative vitreoretinal disorders.

METHODS

In a prospective study of 101 consecutive patients, vitreous and paired serum samples were obtained from 38 patients with rhegmatogenous retinal detachment complicated by proliferative vitreoretinopathy, 25 patients with rhegmatogenous retinal detachment with no proliferative vitreoretinopathy, and 38 patients with proliferative diabetic retinopathy. Gelatinase activities were determined by quantitative zymography.

RESULTS

All vitreous samples contained comparable levels of the constitutive gelatinase A. Inducible gelatinase B was detected in eight (32%) of 25 vitreous samples from patients with rhegmatogenous retinal detachment with no proliferative vitreoretinopathy (mean +/- SD, 319.5 +/- 521.0 scanning units), in 17 (44.7%) of 38 vitreous samples from patients with proliferative vitreoretinopathy (560.6 +/- 718.9 scanning units), and in 34 (89.5%) of 38 vitreous samples from patients with proliferative diabetic retinopathy (1,707.2 +/- 1,220.3 scanning units). The incidence of detection of gelatinase B in proliferative diabetic retinopathy cases was significantly higher than it was in rhegmatogenous retinal detachment with no proliferative vitreoretinopathy and proliferative vitreoretinopathy cases (P < .001). Gelatinase B levels in the vitreous samples of patients with proliferative diabetic retinopathy were higher than the levels found in patients with rhegmatogenous retinal detachment with no proliferative vitreoretinopathy and in patients with proliferative vitreoretinopathy (P = .0152). Gelatinase A was detected in all the tested sera, whereas none of the tested paired serum samples contained detectable gelatinase B activity.

CONCLUSIONS

Gelatinase B may play an important role in extracellular matrix degradation associated with neovascularization in proliferative diabetic retinopathy.

摘要

目的

研究明胶酶A和B是否参与增殖性玻璃体视网膜病变的发病机制。

方法

在一项对101例连续患者的前瞻性研究中，从38例伴有增殖性玻璃体视网膜病变的孔源性视网膜脱离患者、25例无增殖性玻璃体视网膜病变的孔源性视网膜脱离患者以及38例增殖性糖尿病视网膜病变患者中获取玻璃体和配对血清样本。通过定量酶谱法测定明胶酶活性。

结果

所有玻璃体样本中组成型明胶酶A的水平相当。在25例无增殖性玻璃体视网膜病变的孔源性视网膜脱离患者的玻璃体样本中，有8例（32%）检测到诱导型明胶酶B（平均±标准差，319.5±521.0扫描单位）；在38例增殖性玻璃体视网膜病变患者的玻璃体样本中，有17例（44.7%）检测到（560.6±718.9扫描单位）；在38例增殖性糖尿病视网膜病变患者的玻璃体样本中，有34例（89.5%）检测到（1707.2±1220.3扫描单位）。增殖性糖尿病视网膜病变病例中明胶酶B的检测发生率显著高于无增殖性玻璃体视网膜病变的孔源性视网膜脱离病例和增殖性玻璃体视网膜病变病例（P<.001）。增殖性糖尿病视网膜病变患者玻璃体样本中的明胶酶B水平高于无增殖性玻璃体视网膜病变的孔源性视网膜脱离患者和增殖性玻璃体视网膜病变患者（P=.0152）。在所有检测的血清中均检测到明胶酶A，而所有检测的配对血清样本中均未检测到可检测到的明胶酶B活性。