Sugiyama Tetsuya, Katsumura Kozo, Nakamura Kimitoshi, Kobayashi Masato, Muramatsu Michiko, Maruichi Midori, Oku Hidehiro, Takai Shinji, Miyazaki Mizuo, Ikeda Tsunehiko
Department of Ophthalmology, Osaka Medical College, 27 Daigaku-cho, Takatsuki, Osaka 569-8686, Japan.
Ophthalmic Res. 2006;38(4):201-8. doi: 10.1159/000093072. Epub 2006 May 4.
To investigate chymase involvement in idiopathic macular hole onset, the effects of chymase on monkey eyes and cultured Muller cells were investigated.
Immunohistochemistry using antinestin and antiglial fibrillary acidic protein antibodies was performed in a normal monkey eye. After chymase was injected into the monkey vitreous, histological changes in the retina were evaluated using the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Expression of c-kit, a stem cell factor receptor, and nestin was examined in porcine Muller cells cultured with basic fibroblast growth factor. The effects of chymase on proliferation and TUNEL staining in Muller cells were also examined.
The number of nestin and glial fibrillary acidic protein-positive cells was higher in the macula than in other regions. Thickening of the posterior hyaloid membrane and some apoptotic cells were found in the macula of chymase-treated eyes. The expression of c-kit and nestin in Muller cells was shown and enhanced when cultured with basic fibroblast growth factor. Exposure to chymase inhibited Muller cell proliferation and produced TUNEL-positive cells.
There might be Muller cells possessing atypical properties near the macular region and chymase might cause fibrosis and apoptosis through these cells. These findings suggest that increased chymase activity may result in idiopathic macular hole onset.
为研究糜酶在特发性黄斑裂孔发病中的作用,对糜酶对猴眼和培养的 Müller 细胞的影响进行了研究。
在正常猴眼中使用抗巢蛋白和抗胶质纤维酸性蛋白抗体进行免疫组织化学。将糜酶注入猴玻璃体后,使用末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记(TUNEL)法评估视网膜的组织学变化。在用碱性成纤维细胞生长因子培养的猪 Müller 细胞中检测干细胞因子受体 c-kit 和巢蛋白的表达。还研究了糜酶对 Müller 细胞增殖和 TUNEL 染色的影响。
黄斑区巢蛋白和胶质纤维酸性蛋白阳性细胞的数量高于其他区域。在经糜酶处理的眼睛的黄斑区发现后玻璃膜增厚和一些凋亡细胞。当与碱性成纤维细胞生长因子一起培养时,Müller 细胞中 c-kit 和巢蛋白的表达被显示并增强。暴露于糜酶会抑制 Müller 细胞增殖并产生 TUNEL 阳性细胞。
黄斑区附近可能存在具有非典型特性的 Müller 细胞,糜酶可能通过这些细胞导致纤维化和凋亡。这些发现表明糜酶活性增加可能导致特发性黄斑裂孔的发生。