Diabetic retinopathy (DR) is a common complication of diabetes, and the leading cause of blindness in adults. Sprouty-related proteins with EVH1 domain (SPRED2) play an important role in diabetes and are closely related to the lens and eye morphogenesis. This study attempted to investigate the role and related mechanism of SPRED2 in DR. DR rat model was established by administration streptozocin. Human retinal endothelial cells (HRECs) were treated with high glucose (HG) to mimic DR. The results showed that SPRED2 expression was decreased in the retinal tissues of DR rats and HG-treated HRECs. MTT assay and flow cytometry data showed that SPRED2 overexpression reduced cell viability of HG-treated HRECs. SPRED2 overexpression enhanced Caspase-3 activity and promoted apoptosis of HG-treated HRECs. Furthermore, the expressions of endothelial cell markers CD31 and E-cad were down-regulated, whereas the expressions of mesenchymal cell markers FSP1, SM22, and α-SMA were up-regulated in the HG-treated HRECs. SPRED2 overexpression reversed HG-induced endothelial–mesenchymal transition in HRECs. The expressions of tight junction components claudin 3, occludin, and ZO-1 were increased in HG-treated HRECs following SPRED2 up-regulation. In addition, SPRED2 overexpression downregulated the expression of p-ERK1/2, p-p38, and p-JNK in the HG-treated HRECs. In conclusion, this study demonstrated that SPRED2 overexpression repressed endothelial–mesenchymal transition and endothelial injury in HG-treated HRECs by suppressing MAPK signaling pathway. These findings suggested that SPRED2 may be a novel potential therapeutic target implicated in DR progression.
Objective To calculate the Q values from the human anterior corneal surface with the tangential radius of curvature and analyze its distribution characteristics in different age and refractive status groups. Methods Tangential power maps of the anterior cornea from Orbscan II were acquired for 201 subjects' right eyes. They were divided into groups of adults and children and then divided further into subgroups according to the refraction status. The Q values of each semimeridian were calculated by the tangential radius with a linear regression equation. The Q value distribution in both the nasal cornea and temporal cornea were analyzed. Results The mean temporal Q values of the emmetropia group of adults and all children's groups were significantly different from the mean nasal Q value. The mean nasal corneal Q values were more negative in children. The adult group showed differences only in the low myopia group. The mean Q value of the nasal cornea among different refractive groups of children was significantly different, and so was the temporal cornea between the adult myopia and emmetropia group. Conclusion The method using the tangential radius of curvature combined with linear regression to obtain anterior surface Q values for both adults and children was stable and reliable. When we analyzed the anterior corneal Q value, area division was necessary.
Diabetic retinopathy (DR) is one of the more serious complications of diabetes. However, the mechanisms involved in DR are complex and still need to be investigated. The beneficial effects of fisetin have been widely reported, but whether it is beneficial in DR is not clear yet. This study was designed to investigate the regulatory role of fisetin in regulating DR and explore the involved mechanism. First, 30 mM glucose was used to establish DR cell model in vitro. Cell counting kit 8 (CCK8) assay was utilized to study the effects of fisetin on cell viability through treating human retinal microvascular endothelial cells (HRMECs) with 25, 50, and 100 μM fisetin. Transwell and wound healing assays were used to detect the function of fisetin on the migration and angiogenesis on HG-induced HRMECs. Finally, OE-VEGF was used as a mimic of VEGF, and western blotting (WB) was used to verify the targeting genes of fisetin. HG induced an increase in cell viability, cell migration, and angiogenesis in HRMECs, whereas fisetin inhibited these enhancements induced by HG through inhibiting VEGF. In conclusion, fisetin prevents angiogenesis in DR by downregulating VEGF.
Purpose: To develop a visual function-based deep learning system (DLS) using fundus images to screen for visually impaired cataracts.Materials and methods: A total of 8,395 fundus images (5,245 subjects) with corresponding visual function parameters collected from three clinical centers were used to develop and evaluate a DLS for classifying non-cataracts, mild cataracts, and visually impaired cataracts. Three deep learning algorithms (DenseNet121, Inception V3, and ResNet50) were leveraged to train models to obtain the best one for the system. The performance of the system was evaluated using the area under the receiver operating characteristic curve (AUC), sensitivity, and specificity.Results: The AUC of the best algorithm (DenseNet121) on the internal test dataset and the two external test datasets were 0.998 (95% CI, 0.996–0.999) to 0.999 (95% CI, 0.998–1.000),0.938 (95% CI, 0.924–0.951) to 0.966 (95% CI, 0.946–0.983) and 0.937 (95% CI, 0.918–0.953) to 0.977 (95% CI, 0.962–0.989), respectively. In the comparison between the system and cataract specialists, better performance was observed in the system for detecting visually impaired cataracts (p < 0.05).Conclusion: Our study shows the potential of a function-focused screening tool to identify visually impaired cataracts from fundus images, enabling timely patient referral to tertiary eye hospitals.
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