PubMed · 7340651
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I S Jain. 1981. Dilantin cataract.. https://pubmed.ncbi.nlm.nih.gov/7340651/
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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: The aim of the study was to evaluate results of visual acuity and binocularity and complications after cataract surgery with primary capsular bag-fixated IOL implantation in children. MATERIALS AND METHODS: Thirty-three children [mean age (+/- SEM) 6.9 +/- 2.9 years, range 3-12 years] accounting for 43 eyes, were examined before and after surgery (15 traumatic, 19 developmental, and 9 congenital cataracts, of the latter two groups 9 unilateral and 19 bilateral cataracts). RESULTS: All eyes had a best corrected postoperative visual acuity of 0.5 +/- 0.05. The postoperative visual acuity of the traumatic cataracts was 0.6 +/- 0.07, of the developmental cataracts 0.5 +/- 0.07, and of the congenital cataracts 0.2 +/- 0.05. Of the 43 eyes, 17 (40%) showed a best corrected visual acuity of 0.5 or better. There was a positive correlation between morphology (lamellar versus subcapsular opacification) and visual acuity (0.7 +/- 0.07 versus 0.5 +/- 0.05; P < 0.05). Bilateral cataracts had a better postoperative visual acuity than unilateral cataracts (0.7 +/- 0.07 versus 0.2 +/- 0.05 P< 0.001) Stereopis was found postoperatively in 62% of the children. In one eye a capsular bag-fixated IOL implantation was not possible, and so the IOL was inserted in the sulcus. Four children presented with postoperative fibrin formation. Posterior capsule opacification occurred in 19% of the eyes in which a primary posterior capsulotomy had been performed. CONCLUSIONS: The prognosis of visual acuity and the results of stereopsis in children older than 3 years following capsular bag-fixated IOL implantation are very good. Both the intraoperative and postoperative complication rates were low.
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