RESUMEN
PURPOSE: To develop a chemical method that makes porcine lens anterior capsule resemble human lens anterior capsule in tear force and perforating force. SETTING: Beijing Tongren Hospital, Beijing, China. DESIGN: Experimental study. METHODS: Porcine eyes were divided into groups, and reagents (0.9% physiological saline, 0.1% sodium hypochlorite, 0.3% sodium hypochlorite, and 0.5% sodium hypochlorite) were injected into the anterior chamber, respectively, recorded as Groups A, B, C, and D, respectively. A senior physician collected each group of anterior capsules after performing continuous circular capsulorhexis and assessing the anterior capsule's tearing and perforation forces. An additional group, which consisted of human lens anterior capsules taken in the operating room from patients with cataract, recorded as Group E. A tensile system was used to measure each sample's tensile force. RESULTS: A significant difference was found between Group A and any other group in maximum tensile force and average tensile force in both transverse and longitudinal directions. No significant difference was found between any 2 groups from Group B to Group E. According to the surgeon's assessment, the tear force characteristic of the porcine lens anterior capsule treated with 0.1%, 0.3%, and 0.5% sodium hypochlorite solution was similar to that of the human lens anterior capsule. CONCLUSIONS: Porcine lens capsule treated using this method can be used for training of new surgeons. The porcine lens anterior capsule treated with 0.5% sodium hypochlorite, which results showed most resembled human lens anterior capsule, can be used for robotic training.
Asunto(s)
Capsulorrexis , Cápsula del Cristalino , Animales , Porcinos , Humanos , Capsulorrexis/métodos , Cápsula del Cristalino/cirugía , Hipoclorito de Sodio/farmacología , Resistencia a la Tracción , Cápsula Anterior del Cristalino/cirugíaRESUMEN
Epithelial mesenchymal transition (EMT) occurring in retinal pigment epithelial cells (RPE) is a crucial mechanism that contributes to the development of age-related macular degeneration (AMD), a pivotal factor leading to permanent vision impairment. Long non-coding RNAs (lncRNAs) have emerged as critical regulators orchestrating EMT in RPE cells. In this study, we explored the function of the lncRNA CYTOR (cytoskeleton regulator RNA) in EMT of RPE cells and its underlying mechanisms. Through weighted correlation network analysis, we identified CYTOR as an EMT-related lncRNA associated with AMD. Experimental validation revealed that CYTOR orchestrates TGF-ß1-induced EMT, as well as proliferation and migration of ARPE-19 cells. Further investigation demonstrated the involvement of CYTOR in regulating the WNT5A/NFAT1 pathway and NFAT1 intranuclear translocation in the ARPE-19 cell EMT model. Mechanistically, CHIP, EMSA and dual luciferase reporter assays confirmed NFAT1's direct binding to CYTOR's promoter, promoting transcription. Reciprocally, CYTOR overexpression promoted NFAT1 expression, while NFAT1 overexpression increased CYTOR transcription. These findings highlight a mutual promotion between CYTOR and NFAT1, forming a positive feedback loop that triggers the EMT phenotype in ARPE-19 cells. These discoveries provide valuable insights into the molecular mechanisms of EMT and its association with AMD, offering potential avenues for targeted therapies in EMT-related conditions, including AMD.
Asunto(s)
Transición Epitelial-Mesenquimal , Retroalimentación Fisiológica , Degeneración Macular , Factores de Transcripción NFATC , ARN Largo no Codificante , Epitelio Pigmentado de la Retina , Transición Epitelial-Mesenquimal/genética , Humanos , Epitelio Pigmentado de la Retina/metabolismo , Epitelio Pigmentado de la Retina/citología , Factores de Transcripción NFATC/metabolismo , Factores de Transcripción NFATC/genética , ARN Largo no Codificante/fisiología , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Degeneración Macular/genética , Degeneración Macular/metabolismo , Degeneración Macular/patología , Degeneración Macular/etiología , Expresión Génica/genética , Proliferación Celular/genética , Movimiento Celular/genética , Factor de Crecimiento Transformador beta1/metabolismo , Transducción de Señal/genética , Transducción de Señal/fisiología , Células Epiteliales/metabolismo , Línea Celular , Células CultivadasRESUMEN
Worldwide, age-related macular degeneration (AMD) is a multifactorial progressive fundus disorder that can cause vision impairment and severe central blindness in older adults. Currently, there are no approved prevention or treatment strategies for non-exudative AMD. While targeting VEGF is the main therapeutic approach to delay the degeneration process in exudative AMD, a significant number of patients show insensitivity or ineffectiveness to anti-VEGF therapy. Despite years of research, the exact mechanism underlying drusen formation and macular atrophy in AMD remains unknown. In the pathogenesis of AMD, lncRNAs play crucial roles, as discussed in this paper. This review focuses on the function of dysregulated lncRNAs and the mechanisms by which specific molecules target these lncRNAs in AMD. The analysis reveals that lncRNAs primarily regulate the progression of AMD by mediating apoptosis, epithelial-mesenchymal transition (EMT), dedifferentiation, and oxidative stress in choroidal vascular endothelial cells, retinal pigment epithelium (RPE) cells, and photoreceptors. Consequently, the regulation of apoptosis, dedifferentiation, EMT, and other processes by lncRNAs has emerged as a crucial focus in AMD research.These findings contribute to our understanding of the role of lncRNAs in AMD and their potential as valuable biomarkers. Furthermore, they highlight the need for further basic and clinical studies to explore the value of lncRNAs as biomarkers and potential therapeutic targets for AMD.