The Role of Inverted Internal Limiting Membrane Flap in Macular Hole Closure
The Role of Inverted Internal Limiting Membrane Flap in Macular Hole Closure
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DOI：
10.1167/iovs.17-21756
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发表时间：
2017-09-01
影响因子：
4.4
通讯作者：
Shiraga, Fumio
中科院分区：
文献类型：
--
作者：
Shiode, Yusuke;Morizane, Yuki;Shiraga, Fumio
目的。目的探讨倒置内界膜(ILM)手术后黄斑裂孔(MH)闭合的机制。方法：采用内界膜倒置手术技术建立猕猴黄斑裂孔(MH)模型，用免疫组织化学方法观察MH闭合的过程。然后，我们研究了IV型胶原、纤维连接蛋白和层粘连蛋白对培养的Muller细胞(MIO-M1)增殖和迁移的影响。通过免疫组织化学染色和实时逆转录聚合酶链式反应，研究神经营养因子和碱性成纤维细胞生长因子在人ILM和MIO-M1细胞中的表达，以及MIO-M1迁移对这些因子表达的影响。结果：内翻性ILM皮瓣手术后10天，MH周围有封闭的和增殖的胶质纤维酸性蛋白(GFAP)阳性细胞。IV型胶原、纤维连接蛋白和层粘连蛋白均可促进MIO-M1细胞的增殖，而IV型胶原和纤维连接蛋白可促进MIO-M1细胞的迁移。神经营养因子和碱性成纤维细胞生长因子存在于人ILM表面，MIO-M1细胞产生这些因子。结论：在MH闭合过程中，ILM作为Muller细胞增殖和迁移的支架，可能促进了Muller细胞的活化。激活的Muller细胞产生的神经营养因子和碱性成纤维细胞生长因子存在于ILM表面，可能有助于MH的关闭。
PURPOSE. To investigate the mechanism of macular hole (MH) closure following the inverted internal limiting membrane (ILM) technique.METHODS. We performed the inverted ILM flap surgical technique as an experimental MH model in monkeys, and investigated the process of MH closure immunohistochemically. We then investigated the effects of type IV collagen, fibronectin, and laminin, which are constituent proteins of the ILM, on the proliferation and migration of cultivated Muller cells (MIO-M1). We also investigated the expression of neurotrophic factors and basic fibroblast growth factor (bFGF) in human ILM and MIO-M1 cells, and the effect of MIO-M1 migration on the expression of these factors, via immunohistochemical staining and the real-time reverse transcription polymerase chain reaction.RESULTS. Ten days after inverted ILM flap surgery, the MH had closed and proliferating glial fibrillary acidic protein (GFAP)-positive cells surrounded the ILM. Type IV collagen, fibronectin, and laminin all enhanced the proliferation of MIO-M1 cells, and type IV collagen and fibronectin enhanced the migration of MIO-M1 cells. Neurotrophic factors and bFGF were present on the surface of the human ILM, and MIO-M1 cells produced these factors. Neurotrophic factors and bFGF were expressed to a significantly greater extent by migrating MIO-M1 cells than by these cells in their static state.CONCLUSIONS. During MH closure, the ILM functioned as a scaffold for the proliferation and migration of Muller cells, and may promote Muller cell activation. Neurotrophic factors and bFGF produced by activated Muller cells and present on the surface of the ILM may contribute to MH closure.