González-Avila G, Ginebra M, Hayakawa T, Vadillo-Ortega F, Terán L, Selman M
Department of Molecular Biology, Instituto Nacional de Enfermedades Respiratorias, México City, México.
Arch Ophthalmol. 1995 Oct;113(10):1319-23. doi: 10.1001/archopht.1995.01100100107039.
To explore the influence of aqueous humor from patients with glaucoma on collagen turnover.
The aqueous humor of patients with primary open-angle glaucoma (POAG), chronic angle-closure glaucoma, congenital glaucoma, neovascular glaucoma, and senile cataract (control group) was analyzed for its capacity to induce fibroblast proliferation, collagen synthesis, collagenolytic activity, and production of tissue inhibitor of metalloproteinase-1. All data were analyzed using the Mann-Whitney U test.
Aqueous humor derived from patients with POAG induced a significant decrease of functional collagenase activity (mean +/- SE, 9.12 +/- 1.33 microgram of degraded collagen per milligram of incubated protein vs 20.94 +/- 4.14 micrograms from the control group, P < .05). The enzymatic activity in the other types of glaucoma was similar to that of controls. The POAG samples had a significantly higher concentration of tissue inhibitor of metalloproteinase-1 (mean +/- SE, 3.11 +/- 0.58 vs 0.91 +/- 0.13 micrograms/mL from controls; P < .05). The amount of immunoreactive tissue inhibitor of metalloproteinase-1 found in the other three groups was not significantly different from the control. Aqueous humor stimulated fibroblast proliferation in all cases, but significant differences were not observed between the POAG samples (mean +/- SE, 20,285 +/- 4642 cpm/mg of incubated protein) and the control group samples (26,550 +/- 3688 cpm/mg of incubated protein). Primary open-angle glaucoma fluids increased collagen synthesis significantly compared with the control group (mean +/- SD, 3352 +/- 630 vs 985 +/- 285, P < .05), and the other groups.
An increase of collagen synthesis and a decrease of collagen degradation may contribute to an excessive deposit of collagen with loss of the trabecular cells during the development of POAG, and aqueous humor must be considered as a microenvironment that affects the metabolism or function of the trabecular meshwork or both.
探讨青光眼患者房水对胶原周转的影响。
分析原发性开角型青光眼(POAG)、慢性闭角型青光眼、先天性青光眼、新生血管性青光眼患者以及老年性白内障患者(对照组)的房水诱导成纤维细胞增殖、胶原合成、胶原olytic活性和金属蛋白酶组织抑制剂-1产生的能力。所有数据采用Mann-Whitney U检验进行分析。
POAG患者的房水导致功能性胶原酶活性显著降低(平均值±标准误,每毫克孵育蛋白降解的胶原为9.12±1.33微克,而对照组为20.94±4.14微克,P<.05)。其他类型青光眼的酶活性与对照组相似。POAG样本中金属蛋白酶组织抑制剂-1的浓度显著更高(平均值±标准误,3.11±0.58微克/毫升,而对照组为0.91±0.13微克/毫升;P<.05)。在其他三组中发现的免疫反应性金属蛋白酶组织抑制剂-1的量与对照组无显著差异。房水在所有情况下均刺激成纤维细胞增殖,但POAG样本(平均值±标准误,每毫克孵育蛋白20,285±4642 cpm)与对照组样本(每毫克孵育蛋白26,550±3688 cpm)之间未观察到显著差异。与对照组(平均值±标准差,3352±630对985±285,P<.05)及其他组相比,原发性开角型青光眼房水显著增加胶原合成。
胶原合成增加和胶原降解减少可能导致POAG发生过程中胶原过度沉积及小梁细胞丢失,房水必须被视为影响小梁网代谢或功能或两者的微环境。