Biological function and mechanism of lncRNA-MEG3 in Tenon’s capsule fibroblasts proliferation: By MEG3-Nrf2 protein interaction

摘要: Abstract Objective The proliferation of Tenon’s capsule fibroblasts after glaucoma filtration surgery is a harmful element for operation failure. However, the underlying mechanism remains unclear. In this study, we evaluated role long non-coding RNA (lncRNA)-MEG3 in Glaucoma (GTFs) with model transforming growth factor-β (TGF-β)-induced which has been used previous studies to explore Methods vitro cell was made by TGF-β2 (5 ng/mL)-stimulated GTFs obtained from patients surgery, and viability assessed MTT assay [3H] thymidine incorporation respectively. Relative expression MEG3 Nrf2 mRNA determined quantitative real-time PCR. protein level detected western blot. Functional interaction between examined pull down Binding Protein Immunoprecipitation (RIP). Results As isolated fibroblasts, both decreased compared control (HTFs). Adenovirus mediated overexpression attenuates ability proliferation, as well contributed upregulation TGF-β2-stimualted GTFs. positively affects rather than mRNA. We found that functional them depends on MEG3-Nrf2 formation RIP analysis also proved be involved TGF-β2-induced proliferation. Conclusion above data suggested lncRNA-MEG3 constitutes induces via direct binding Nrf2.