Amniotic membrane transplantation promotes retinal hole closure in a rabbit model
Abstract
Amniotic membrane transplantation (AMT) is an effective treatment for refractory macular hole closure, yet the underlying mechanism supporting that effectiveness remains unclear. Here, we investigated the role of retinal regeneration in this process using an in vivo rabbit retinal-hole (RH) model in which AMT was performed on one of the holes. Histological and immunofluorescence examinations with anti-glial fibrillary acidic protein and anti-glutemine synthetase antibodies were conducted to evaluate cell migration and hole closure. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to analyze the tissues after implantation. Optical coherence tomography scans revealed that AMT promoted RH closure. Histological analyses demonstrated that retinal pigment epithelium (RPE) cells migrated onto the AM, and immunofluorescence analyses showed that retinal glial cells, including Müller cells, contributed to RH closure. SEM and TEM findings revealed cellular coverage and extracellular matrix formation at the AMT site, suggesting successful integration with the surrounding retinal tissue. Furthermore, the loss of mitochondrial cristae within the RPE caused by the creation of RH was suppressed by AMT. In summary, AMT promoted RH closure in a rabbit model by serving as a scaffold for retinal cell migration and by preserving RPE integrity, although regeneration of the retinal-layers was not observed.
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