Hisatomi Toshio, Enaida Hiroshi, Sakamoto Taiji, Kanemaru Takaaki, Kagimoto Tadahisa, Yamanaka Ichiro, Ueno Akifumi, Nakamura Takao, Hata Yasuaki, Ishibashi Tatsuro
Department of Ophthalmology and Morphology Core, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Arch Ophthalmol. 2006 Jul;124(7):1005-11. doi: 10.1001/archopht.124.7.1005.
To elucidate the pathogenesis of macular hole formation, focusing in particular on the possible role of cellular migration on the cortical vitreous and internal limiting membrane (ILM) around the macular hole.
To gain a comprehensive overview of the ILM excised in macular hole surgery (n = 36), the ILMs were carefully unfolded and spread out onto glass slides as continuous flat sheets that each contained a macular hole. The specimens were observed by light microscopy and transmission electron microscopy (n = 9), and the cellular distribution was analyzed by scanning electron microscopy in a quantitative manner (n = 27). Immunohistochemistry for glial fibrillary acidic protein and cytokeratin 18 was carried out for cellular characterization. Cellular proliferation was assessed by immunohistochemistry for proliferating cell nuclear antigen and Ki-67.
Cellular migration was not apparent around the macular hole in the early stage of development of the macular hole (stage 2, 0 microm). As the macular hole passed through the later stages of development, cellular migration developed around the macular hole (stage 3, 84 microm) and the area of cellular migration gradually enlarged (stage 4, 420 microm). The immunophenotypic analysis showed that these cells were mainly glial fibrillary acidic protein-positive glial cells and cytokeratin 18-positive retinal pigment epithelial cells. The proliferating cell nuclear antigen and Ki-67 immunohistochemistry showed that some of these cells were proliferating on the ILM.
Cellular migration on the ILM is not necessary for the initial formation of a macular break. Cellular migration developed after the macular break occurred, and the migration and proliferation increased gradually from the macular hole.
This study provides a new method for understanding the ultrastructural analysis of the pathogenesis of the macular hole.
阐明黄斑裂孔形成的发病机制，尤其关注细胞迁移在黄斑裂孔周围皮质玻璃体和内界膜（ILM）上可能发挥的作用。
为全面了解黄斑裂孔手术中切除的ILM（n = 36），将ILM小心展开并平铺在载玻片上，形成每张都包含一个黄斑裂孔的连续平片。通过光学显微镜和透射电子显微镜观察标本（n = 9），并采用扫描电子显微镜对细胞分布进行定量分析（n = 27）。进行胶质纤维酸性蛋白和细胞角蛋白18的免疫组织化学检测以对细胞进行特征鉴定。通过增殖细胞核抗原和Ki-67的免疫组织化学检测评估细胞增殖情况。
在黄斑裂孔发育的早期阶段（2期，0微米），黄斑裂孔周围未观察到明显的细胞迁移。随着黄斑裂孔进入发育后期，黄斑裂孔周围出现细胞迁移（3期，84微米），且细胞迁移区域逐渐扩大（4期，420微米）。免疫表型分析表明，这些细胞主要是胶质纤维酸性蛋白阳性的神经胶质细胞和细胞角蛋白18阳性的视网膜色素上皮细胞。增殖细胞核抗原和Ki-67免疫组织化学检测显示，其中一些细胞在ILM上增殖。
ILM上的细胞迁移对于黄斑裂孔的初始形成并非必要。细胞迁移在黄斑裂孔形成后出现，且从黄斑裂孔开始迁移和增殖逐渐增加。
本研究为理解黄斑裂孔发病机制的超微结构分析提供了一种新方法。
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