Fei Zhao

Ludwig-Maximilian-University of Munich, München, Bavaria, Germany

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Publications (3)9.3 Total impact

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    ABSTRACT: PURPOSE:: To describe new details of epiretinal cell proliferation in flat-mounted internal limiting membrane specimens. METHODS:: One hundred nineteen internal limiting membrane specimens were removed en bloc with epiretinal membranes from 79 eyes with macular pucker (MP) and 40 eyes with vitreomacular traction syndrome. Intraoperatively, posterior vitreous detachment was assessed as complete or incomplete. Whole specimens were flat-mounted on glass slides and processed for interference and phase-contrast microscopy, cell viability assay, and immunocytochemistry. RESULTS:: Mean cell viability percentage was higher in MP than in vitreomacular traction syndrome. Two cell distribution patterns were found. Anti-CD163 labeling presented predominantly in MP with complete posterior vitreous detachment. CD45 expression was similar in all groups of diagnosis. Anti-glial fibrillary acidic protein (GFAP) labeling was found in MP irrespective of the extent of posterior vitreous detachment. Alpha-SMA (α-smooth muscle actin) labeling was mainly presented in MP with incomplete posterior vitreous detachment and in vitreomacular traction syndrome. Simultaneous antibody labeling included GFAP/CD45, GFAP/CD163, CD163/CD45, and CD163/α-SMA. CONCLUSION:: Hyalocytes constitute a major cell type of epiretinal cell proliferation in eyes with MP and vitreomacular traction syndrome. Glial cells, notably retinal Muller cells, are involved as well. It appears that transdifferentiation of cells in vitreomacular traction might be more frequent than previously thought and that those cells possess a greater variability of immunocytochemical properties than expected.
    Retina (Philadelphia, Pa.) 08/2012; · 2.93 Impact Factor
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    ABSTRACT: To provide pathology data on the completeness of epiretinal membrane (ERM) removal with and without internal limiting membrane (ILM) peeling. Twenty-two patients with idiopathic ERM formation underwent vitrectomy with ERM removal and subsequent staining of the vitreomacular interface with brilliant blue. If the ILM was still present after ERM removal, it was peeled off. Both ERM and ILM specimens were harvested in different containers and prepared for flat-mount phase-contrast and interference microscopy, immunocytochemistry, and transmission electron microscopy. In 14 patients (64%), the ILM was still present at the macula after ERM removal. On average, 20% (range, 2-51%) of the total cell count was left behind at the ILM if the ERM was removed only. There were mainly glial cells on the ILM, and few hyalocytes. In nine eyes, the cells were forming cell clusters. In 8 patients (36%), both ERM and ILM were removed together. Electron microscopy showed cellular proliferation directly attached to the ILM in these eyes, whereas in the sequentially peeled group, there was collagen interposed between the ERM and the ILM. Surgical ERM removal resulted in splitting of the vitreous cortex in these eyes, leaving the ILM with residual cells behind. Simple ERM removal results in sufficient separation of fibrocellular tissue in one third of cases, only. In 2 of 3 patients with idiopathic ERM, the vitreous cortex splits when the ERM is removed, leaving an average of 20% of the total cell count behind on the ILM. As these cells are capable of proliferation and causing ERM recurrence, staining of the ILM with subsequent removal seems beneficial in macular pucker surgery.
    Retina (Philadelphia, Pa.) 11/2011; 32(3):477-85. · 2.93 Impact Factor
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    ABSTRACT: To provide new information on epiretinal cell proliferation and the cells' origin in idiopathic macular holes and to overcome the effects of embedding and sectioning preparation procedures on cell-distribution patterns. Interference and phase-contrast microscopy, immunocytochemistry, and scanning and transmission electron microscopy were performed on surgically excised whole-mounted internal limiting membrane (ILM) specimens removed from 60 eyes with idiopathic macular holes. Cell distribution and cell morphology were correlated with immunocytochemical staining characteristics. Twelve cell type-specific antibodies were used to detect glial cells, hyalocytes, retinal pigment epithelial cells, retinal ganglion cells, and immune cells. Cell viability was analyzed. Epiretinal cell proliferation was found in all ILM specimens, irrespective of the stage of the macular hole. Cell density showed a broad variety. Immunocytochemistry frequently revealed simultaneous expression of GFAP/CD45, GFAP/CD64, GFAP/CD68, GFAP/CRALBP, and GFAP/CD90. Some cells presented with intracellular contractile filaments (anti-αSMA); others were not immunoreactive to any antibody examined. The percentage of viable cells showed a broad variety with a mean of 73% (SD 29%). Electron microscopy demonstrated glial cells, hyalocytes, and myofibroblast-like cells. The presence of epiretinal cells at the ILM in all macular hole stages strongly suggests a substantial involvement of cell migration and proliferation in the course of macular hole development. Glial cells and hyalocytes play the predominant role in epiretinal cell proliferation. Given the co-expression of glial cell and hyalocyte markers, transdifferentiation of epiretinal cells needs further elucidation, especially with respect to αSMA-positive cells leading to traction at the vitreoretinal interface.
    Investigative ophthalmology & visual science 09/2011; 52(11):7822-34. · 3.43 Impact Factor