PubMed · 13239338
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
E REGNIER. 1955. Developmental cataract.. https://pubmed.ncbi.nlm.nih.gov/13239338/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
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.
Explore the source record for details and available documents.
BACKGROUND: Oculocerebrorenal syndrome is an X-linked recessive hereditary oculocerebrorenal disorder characterized by congenital cataract, mental retardation, and Fanconi syndrome of the proximal renal tubules. Other ocular findings include glaucoma, corneal opacity (keloid), enophthalmos, and hypotonia. OBJECTIVE: To describe the treatment of 7 patients (14 eyes) with bilateral cataracts associated with oculocerebrorenal syndrome. Method Retrospective review. RESULTS: Seven patients with oculocerebrorenal syndrome had visually significant bilateral cataracts detected on their first full ophthalmic examination. All underwent bilateral cataract surgery. The mean age (of 14 eyes) at cataract extraction was 1.25 (median, 1.1) months. Glaucoma diagnosis and treatment were more variable. The mean age (of 11 eyes) at glaucoma diagnosis was 24.1 (range, 0.2-70.0) months: the mean age was 0.2 month (of 4 eyes) when glaucoma was diagnosed before cataract extraction, and the mean age was 37.7 months (of 7 eyes) when glaucoma was diagnosed after cataract extraction. All eyes were followed up for a mean of 100.8 (range, 38-190) months. Main Outcome Measure Treatment of 7 patients (14 eyes) with bilateral cataracts associated with oculocerebrorenal syndrome. CONCLUSIONS: Early identification and surgical removal of cataracts is recommended in patients with oculocerebrorenal syndrome. Despite this, visual acuity results will only rarely be better than 20/70, and nystagmus is likely. Patients should be monitored closely and regularly for changes in intraocular pressure, optic nerve cupping, and refractive error to rule out the development of glaucoma.