PubMed · 5612720
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L Calmettes, F Deodati. 1967. [Glaucoma and cataract].. https://pubmed.ncbi.nlm.nih.gov/5612720/
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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.
PURPOSE: To evaluate the preliminary results of stereotactic radiotherapy in the management of patients with juxtapapillary choroidal melanoma. METHODS & MATERIALS: A retrospective, consecutive case series of 28 patients with choroidal melanoma located within 2 mm of the optic nerve who were treated with stereotactic radiotherapy at Princess Margaret Hospital, Toronto, between October 1998 and May 2001. RESULTS: Median age was 62 years. Median tumor height was 4.6 mm and median maximum tumor diameter was 9.4 mm. The prescribed radiation dose was 70 Gy in five fractions over 10 days and median follow-up was 18.5 months. Posttreatment, 2 patients developed local tumor regrowth and 3 patients developed liver metastases. Actuarial rates of local tumor control, metastases, and survival at 18 months were 96%, 10%, and 94%, respectively. Actuarial rates of radiation-induced neovascular glaucoma, cataract, retinopathy, and optic neuropathy at 18 months were 20%, 29%, 30%, and 37%, respectively. A higher radiation dose to the lens was associated with an increased risk of cataract (p = 0.02). CONCLUSIONS: Stereotactic radiotherapy offers a noninvasive alternative to enucleation and brachytherapy in the management of juxtapapillary choroidal melanoma. However, further efforts are needed to optimize local tumor control and minimize radiation-induced complications.
PURPOSE: To identify ultrastructure changes and genetic defects associated with a special fasciculiform autosomal dominant congenital cataract (ADCC) affecting a large Chinese family. METHODS: Members of the Chinese family affected by this special fasciculiform ADCC were studied. Clinical examinations, light and transmission electron microscopy of the removed lens tissue, linkage analyses using polymorphisms of microsatellite markers, and mutational analyses of candidate genes by direct sequencing were performed. RESULTS: The thirteen affected individuals in the family showed no variability between one another. The lens fiber cells showed focal degeneration, dense globular intracellular deposits, and an enlarged intercellular space. This ADCC was associated with a locus on chromosome 2q33-35 (maximum lod score [Zmax]=3.34; theta=0.05). Mutational analyses of the candidate genes (gamma-crystallin; CRYG), identified a C->A heterozygous transversion at nucleotide position 70 in the gammaD-crystallin gene (CRYGD) exon2, which co-segregated with the presence of ADCCs and was not observed in 100 unrelated controls. CONCLUSIONS: This study identified ultrastructure changes and genetic defects associated with a special fasciculiform ADCC affecting a large Chinese family. It appeared to be caused by a missense mutation in the CRYGD gene, further supporting the notion that alterations to CRYG play an important factor in human cataract formation.