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Purpose: To report the surgical outcome of pars plana vitrectomy (PPV) without internal limiting membrane (ILM) peeling in three highly myopic patients with macular retinoschisis and associated posterior staphyloma.
Methods: We report three highly myopic patients with macular retinoschisis and foveal detachment who underwent simple PPV without ILM peeling, with long‐acting gas tamponade. Main outcome evaluations included best corrected visual acuity, biomicroscopic appearance and optical coherence tomography findings.
Results: Pars plana vitrectomy without ILM peeling resulted in anatomic and functional improvement in all three operated eyes for follow‐up periods of ≥ 12 months.
Conclusions: Pars plana vitrectomy without ILM peeling is effective for treating macular retinoschisis and foveal detachment in highly myopic eyes with posterior staphyloma. Visual and anatomic outcomes are comparable with those in previous studies in which ILM removal was performed.
Cell signaling mediated by the αv integrin plays a pivotal role in macrophage activation in various inflammatory processes, but its involvement in the pathogenesis of dry eye disease (DED) remains unclear. In a murine model of DED, we found increased αv integrin expression in ocular surface macrophages. The αv integrins inhibitor c(RGDfK) ameliorated the corneal damage caused by DED, suggesting a pathogenic role for αv integrin. Because tear hyperosmolarity induces ocular inflammation in DED, a hyperosmolar culture of murine bone marrow-derived macrophages (BMDMs) is used to reproduce inflammation in vitro. However, the expression of proinflammatory cytokine mRNA was minimal, even though αv integrin was induced. In searching for components that are involved in αv integrin-mediated inflammation but that are missing from the culture model, we showed that the levels of vitronectin (VTN), a binding ligand of αv integrins, were increased in the tear fluid and conjunctival stroma of DED animals. The addition of VTN prominently enhanced hyperosmolarity-induced inflammation in BMDMs. Mechanistically, we showed that VTN/αv integrins mediated NF-κB activation to induce inflammatory gene expression in the BMDMs. Our findings indicate that interaction the of VTN with αv integrins is a crucial step in the inflammatory process in DED and suggests a novel therapeutic target.
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