PubMed · 14894987
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L BENTOLILA, J M VILA ORTIZ, E V BERTOTTO. Allergic cataract.. https://pubmed.ncbi.nlm.nih.gov/14894987/
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PURPOSE: Traumatic cataract is a common blinding eye disease after ocular trauma, and its pathogenesis is closely related to lens epithelial cell dysfunction, while the definite molecular regulatory mechanism between upstream transcription factor and downstream target gene remains poorly clarified. This study aimed to clarify the role and molecular mechanism of the krüppel-like factor 5 (KLF5)/ thrombosponin 1 (THBS1) axis in regulating proliferation, migration, epithelial-mesenchymal transition and autophagy of lens epithelial cells in traumatic cataract, and to explore its potential clinical therapeutic value. METHODS: The GSE295383 dataset in the gene expression omnibus (GEO) database was downloaded, and the differentially expressed genes (DEGs) were screened by linear models for microarray data (limma) package of R language. Combined with Weighted gene co-expression network analysis (WGCNA), the gene co-expression network was constructed and the key modules were screened. Gene ontology (GO), kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA) combined with human transcription factor target (hTFtarget) and JASPAR databases were used to predict the upstream transcription factors of THBS1. Subsequently, SRA01/04 cells were induced with transforming growth factor-beta 2 (TGF-β2) to construct a cataract cell model. RESULTS: THBS1 and KLF5 were highly expressed in LECs exposed to TGF-β2. KLF5 could activate THBS1 transcription by binding to THBS1 promoter - 174 to -165 sites. Knockdown of THBS1 inhibited TGF-β2-induced viability, proliferation, migration, and altered the expression of epithelial-mesenchymal transition (EMT)- and autophagy-related markers in LECs. Knockdown of KLF5 downregulated THBS1 expression and produced a similar inhibitory effect, while overexpression of THBS1 reversed the effect of KLF5 knockdown. CONCLUSIONS: This study demonstrated that KLF5 promoted the proliferation, migration, and EMT‑associated molecular changes of LECs in traumatic cataract through transcriptional activation of THBS1, and regulated the expression of autophagy‑related markers in LECs, suggesting that KLF5/THBS1 axis might be a potential target for the treatment of traumatic cataract.
BACKGROUND: This paper presents and tests a comprehensive computerised system of analysis of digital images of posterior capsule opacification (PCO). It updates and expands significantly on a previous presentation to include facilities for selecting user defined central areas and for registering and subsequent merging of images for artefact removal. Also, the program is compiled and thus eliminates the need for specialised additional software. The system is referred to in this paper as the open-access systematic capsule assessment (OSCA). The system is designed to be evidence based, objective and openly available, improving on current systems of analysis. METHODS: Principal features of the OSCA system of analysis are discussed. Flash artefacts are automatically located in two PCO images and the images merged to produce a composite free from these artefacts. For this to be possible the second image has to be manipulated with a registration technique to bring it into alignment with the first. Further image processing and analysis steps use a location-sensitive entropy based texture analysis of PCO. Validity of measuring PCO progression of the whole new system is assessed along with visual significance of scores. Reliability of the system is assessed. RESULTS: Analysis of PCO by the system shows ability to detect early progression of PCO, as well as detection of more visually significant PCO. Images with no clinical PCO produce very low scores in the analysis. Reliability of the system of analysis is demonstrated. CONCLUSION: This system of PCO analysis is evidence-based, objective and clinically useful. It incorporates flash detection and removal as well as location sensitive texture analysis. It provides features and benefits not previously available to most researchers or clinicians. Substantial evidence is provided for this system's validity and reliability.
A patient with early bilateral nuclear cataracts and subsequent diagnosis of Fanconi-Bickel syndrome is described. Despite impaired galactose and glucose metabolism, cataracts have been reported in only few cases with this disorder. We conclude that Fanconi-Bickel syndrome should be considered in the differential diagnosis of neonatal cataracts. The pathogenesis of this complication has not been fully elucidated.