Schubert H D, Kuang K, Kang F, Head M W, Fischbarg J
Department of Ophthalmoloy, Columbia University, New York, USA.
Graefes Arch Clin Exp Ophthalmol. 1997 Aug;235(8):523-9. doi: 10.1007/BF00947011.
Retinal glia may play an important role in the closure of macular holes. This in vitro study examines whether and how the specific pathoanatomy, including foveal eversion and foveal vitreous, may interfere with glial closure of macular holes.
Culture dishes used to grow glial cells were modified by the placement of slopes, vertical steps, and gaps to mimic the in vivo migratory surface in and surrounding macular holes. In separate experiments, defects were made in a rodent glial monolayer. These defects were exposed to hyaluronic acid (HA) and to rabbit (RV) and bovine (BV) vitreous gel. The migratory behavior and completeness of closure of defects were compared to controls.
As expected, glial cells migrated further and in greater numbers on a smooth surface. Slopes and steps were moderate obstacles to migration; gaps in the surface were absolute obstacles. HA modified the pattern of adhesion of cells at the bottom of defects. Defects in the glial monolayer were repaired in 5-7 days. Compared to these controls, repair was inhibited by 11% (n.s.), 28% (P = 0.02), and 58% (P = 0.004) after direct exposure of defects to HA, RV and BV, respectively.
The elevated and everted margins of macular holes represent slope, step, and gap-like obstacles to the migration of glial cells and hence to the healing of defects. The defect allows extension of extracellular matrix into it and the subretinal space. Our results indicate that gaps in the migratory surface caused and aggravated by eversion and the presence of vitreous present obstacles to glial migration and closure of macular holes.
视网膜神经胶质细胞可能在黄斑裂孔闭合过程中发挥重要作用。本体外研究旨在探讨包括黄斑中心凹翻转和黄斑中心凹玻璃体在内的特定病理解剖结构是否以及如何干扰黄斑裂孔的神经胶质细胞闭合。
通过设置斜坡、垂直台阶和间隙来对用于培养神经胶质细胞的培养皿进行改造,以模拟黄斑裂孔及其周围的体内迁移表面。在单独的实验中,在啮齿动物神经胶质细胞单层上制造缺损。将这些缺损暴露于透明质酸(HA)、兔(RV)和牛(BV)玻璃体凝胶中。将缺损的迁移行为和闭合完整性与对照组进行比较。
正如预期的那样,神经胶质细胞在光滑表面上迁移得更远且数量更多。斜坡和台阶对迁移是中等障碍;表面的间隙是绝对障碍。HA改变了缺损底部细胞的黏附模式。神经胶质细胞单层缺损在5 - 7天内修复。与这些对照组相比,将缺损分别直接暴露于HA、RV和BV后,修复受到11%(无统计学意义)、28%(P = 0.02)和58%(P = 0.004)的抑制。
黄斑裂孔升高和翻转的边缘对神经胶质细胞迁移以及缺损愈合而言代表着斜坡、台阶和类似间隙的障碍。缺损允许细胞外基质延伸至其中以及视网膜下间隙。我们的结果表明,由翻转导致并加重的迁移表面间隙以及玻璃体的存在对神经胶质细胞迁移和黄斑裂孔闭合构成障碍。