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Introduction: Asthma has been attributed to Th1/Th2 imbalance and inappropriate Th2 responses to environmental allergens. MicroRNAs (miRNAs), 21 to 23 RNA molecules, are first found in mammals and have been implicated in various biological activities. Our previous study found that miR-410 effectively ameliorates airway inflammation in the ovalbumin (OVA)-induced asthma murine model. However, the role of miR-410 in regulating helper T (Th) cell differentiation is not clear. In the present study, we aimed to explore the regulatory effects of miR-410 on the differentiation of Th cells through both in vivo and in vitro studies. Methods: Dual-luciferase reporter assay was used to find if miR-410 has any direct binding position with VEGF mRNAs. PBMC and CD4+ T cells were isolated and stimulated with OVA. The miR-410 mimics and inhibitors were transfected into CD4+ T cells. The differentiation of Th cells was evaluated by enzyme-linked immunosorbent assay (ELISA) for the concentration of IL-4, IFN-γ, and TGF-β levels in supernatants. Western Blot was used to detect protein expression and phosphorylation of PI3K and AKT. BALB/c mice were kept in a specific pathogen-free condition and received sterile OVA-free food and water. OVA-induced asthmatic mice model was established. ELISA was used to measure the bronchoalveolar lavage fluid (BALF) concentrations of IL-4, IFN-γ, TGF-β, and VEGF. Hematoxylin and eosin staining and immunohistochemical staining were conducted to analyze inflammatory cell infiltration, pathological changes, and the expression of VEGF. Results: Dual-luciferase reporter assay showed that miR-410 has no direct binding position with VEGF mRNAs. In the OVA-primed mononuclear cells compared to normal cells, IFN-γ and TGF-β were decreased while IL-4 and VEGF were increased. This change was reversed while miRNA-410 mimics were transfected into CD4+ T cells. Besides, the OVA-primed CD4+ T cells treated with miR-410 decrease the proliferation of cytokine of Th2 cells as well as phosphorylation of PI3K, and AKT. In OVA-induced asthma mice, IFN-γ and TGF-β were decreased in BALF while the IL-4 and VEGF were increased. OVA-induced mice with asthma treated with miR-410 mimics showed marked reductions in the infiltration of inflammatory cells as well as IL-4 and VEGF in BALF. The immunohistochemical staining of the expression of VEGF also decreased in OVA-induced asthma mice with the instillation of miR-410. Conclusions: In this study, we revealed that miR-410 could regulate the differentiation of Th cells via the PI3K-AKT-VEGF signaling pathway in asthma. [ABSTRACT FROM AUTHOR]

Purpose: This study was undertaken to assess the associations between the anatomic outcomes of patients who underwent vitrectomy for rhegmatogenous retinal detachment associated with choroidal detachment (RRDCD) and their preoperative variables. Methods: A total of 175 patients with RRDCD who underwent vitrectomy in one eye were included in the analysis. The primary outcome measured was the retinal status after primary vitrectomy and at the end of follow-up. Results: The retinal reattachment rate was 72.57% after primary surgery, and the final total reattachment rate was 89.14% after follow-up. Binary logistic regression analysis identified that the retinal reattachment rate after primary vitrectomy was significantly associated with older age (odds ratio = 1.03, p = 0.02), mild proliferative vitreoretinopathy (PVR) (PVR grade C vs. PVR grades A-B: odds ratio = 0.31, p = 0.04; PVR grade D vs. PVR grades A-B: odds ratio = 0.03, p < 0.01), and intravitreal steroid treatment (odds ratio = 4.60, p = 0.02), and that the final retinal reattachment rate was independently associated with older age (odds ratio = 1.05; p = 0.01). Conclusions: Vitrectomy is a good surgical option for RRDCD. Older age, mild preoperative PVR, and perioperative intravitreal triamcinolone acetonide injections increase the primary reattachment rates after one operation. Older age was the only independent prognostic factor for the final retinal reattachment in patients with RRDCD. [ABSTRACT FROM AUTHOR]