PubMed · 14927210
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B B LAL DIXIT. 1951. Cataract.. https://pubmed.ncbi.nlm.nih.gov/14927210/
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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.
OBJECTIVE: To present the first reported case of cataract formation as a consequence of instillation of pilocarpine in an eye with a posterior chamber phakic intraocular lens (IOL). DESIGN: Interventional case report. INTERVENTION: A 46-year-old man received a hyperopic implantable collamer lens (ICL) bilaterally. MAIN OUTCOME MEASURES: Determination of best-corrected visual acuity (BCVA); contrast sensitivity testing with and without glare; and intraocular pressure (IOP), specular endothelial cell, and slit-lamp examinations were performed serially. In addition, the distance between the ICL and crystalline lens was measured with optical coherence tomography. RESULTS: Both eyes underwent uneventful ICL implantation for the correction of a manifest spherical equivalent of +7 diopters (D) in the right eye and +7.1 D in the left eye. The left eye was followed for 2 years without developing complications. The right eye, however, showed on the first postoperative day a fleckenlike opacification on the anterior pole of the crystalline lens after instillation on the operative day of 2% pilocarpine in an attempt to accelerate recovery from unwanted pupil dilation causing patient complaints of glare disability after surgery. Optical coherence tomography demonstrated complete contact of the ICL with the natural lens 24 hours postoperatively. Serial IOP measurements were always within the normal limits. The instillation of 1% cyclopentolate resulted in an increase in the ICL vault that measured 132 mum 24 hours later. Three days after the completion of a 3-day course of topical 1% cyclopentolate, the opacification was less dense and demarcated, and a 124-mum vault was measured. Three months postoperatively, the cataract was associated with a 3-line loss of BCVA and considerable degradation of the contrast sensitivity, especially at higher spatial frequencies and with a glare source, and corneal endothelial cell changes were within normal limits. One year after ICL implantation, the right eye had to undergo phacoemulsification and IOL implantation, which were uneventful. CONCLUSIONS: Posterior chamber flattening with resulting crystalline lens opacification can occur immediately after the instillation of pilocarpine in an eye with a hyperopic ICL. Therefore, caution should be taken with the administration of cholinergic agonists such as pilocarpine in patients with phakic IOLs, at least if they are hyperopic ICLs.
Lens alpha-crystallin is an oligomeric protein with a molecular mass of 500-1000 kDa and a polydispersed assembly. It consists of two types of subunits, alphaA and alphaB, each with a molecular mass of 20 kDa. The subunits also form homo-oligomers in some other tissues and in vitro. Their quaternary structures, which are dynamic and characterized by subunit exchange, have been studied by many techniques, including fluorescence resonance energy transfer (FRET) and mass spectrometry analysis. The proposed mechanism of subunit exchange has been either by dissociation/association of monomeric subunits or by rapid equilibrium between oligomers and suboligomers. To explore the nature of subunit exchange further, we performed additional FRET measurements and analyses using a fluorescent dye-labeled W9F alphaA-crystallin as the acceptor probe and Trp in other crystallins (wild-type and R116C alphaA, wild-type and R120G alphaB, wild-type and Q155* betaB2) as the donor probe and calculated the transfer efficiency, Förster distance, and average distance between two probes. The results indicate only slight decreased efficiency and increased distance between two probes for the R116C alphaA and R120G alphaB mutations despite conformational changes.