The purpose of this study was to investigate the role of a human lens microRNA (miR-497-5p) in regulating epithelialmesenchymal transition (EMT) under the control of transforming growth factor beta (TGF-β). A microRNA array was used to evaluate the microRNA profiles of untreated and TGF-β-treated human lens epithelial cells in culture. This showed that TGF-β treatment led to the upregulation of 96 microRNAs and downregulation of 39 microRNAs. Thirteen microRNAs were predicted to be involved in the pathogenesis of posterior capsule opacification (PCO). Meanwhile, overexpression of miR-497-5p suppressed cell proliferation and EMT 48 h post-transfection, and inhibition of miR-497-5p accelerated cell proliferation and EMT. Treatment with TGF-β inhibited the expression of miR-497-5p, but not cell proliferation. miR-497-5p was also found to regulate the level of CCNE1 and FGF7, which are reported to be actively involved in EMT. CCNE1 and FGF7 were bona fide targets of miR-497-5p. The results suggest that miR-497-5p participates in the direct regulation of lens epithelial cell EMT and is regulated by TGF-β. miR-497-5p may be a novel target for PCO therapy.
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http://dx.doi.org/10.1007/s11427-019-1603-y | DOI Listing |
Graefes Arch Clin Exp Ophthalmol
January 2025
National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, 270 Xueyuan West Road, Wenzhou, 325027, Zhejiang, China.
Purpose: To investigate whether in diabetic cataract (DC), FoxO1 regulates high glucose (HG)-induced activation of NLRC4/IL-6 inflammatory mediators in human lens epithelial cells (SRA01/04) via the JAK1/STAT1 pathway, leading to cataract formation.
Methods: Expression levels of FoxO1, inflammatory factor IL-6 and inflammatory vesicle NLRC4 were examined in SRA01/04 under high glucose (HG) stress at 25-150 mM. Rat lenses were also cultured using HG medium with or without the addition of the FoxO1 inhibitor AS1842856 and the JAK1 agonist RO8191.
Cont Lens Anterior Eye
January 2025
Department of Regeneration and Cell Therapy, Andalusian Molecular Biology and Regenerative Medicine Centre (CABIMER), Avda. Américo Vespucio 24, 41092 Seville, Spain.
Purpose: To evaluate the role of contact lenses (CLs) in visual rehabilitation following keratoplasty.
Methods: Four databases, including PubMed, Scopus, Web of Science, and Embase were systematically searched for studies published between January 2010 and July 2023. Visual outcomes, daily wearing duration, subjective comfort, rate and etiology of CL discontinuation, corneal endothelial cell density, central corneal thickness, and complications were extracted.
Eye Contact Lens
January 2025
Medical College of Wisconsin, Milwaukee, WI.
Purpose: To describe a rare case of infectious keratitis secondary to Brevundimonas diminuta, a gram-negative bacillus with fluoroquinolone resistance and rare clinical isolation.
Methods: A 50-year-old man with contact lens overuse presented with a large corneal ulcer and hand motion visual acuity. Initial treatment with fortified topical tobramycin and vancomycin yielded slow improvement, and initial culture grew Staphylococcus epidermidis, Staphylococcus hominis, and Corynebacterium bovis.
J Biochem Mol Toxicol
February 2025
Department of Ophthalmology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Age-related cataracts (ARCs) are associated with increased oxidative stress and cellular senescence. Our objective is to investigate the function of Sirtuin 1 (SIRT1) within ARCs. In ARCs tissues and HO-treated lens epithelial cells (LECs), the expression levels of SIRT1 were examined.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 102446, China. Electronic address:
Age-related cataract (ARC) remains the leading cause of blindness worldwide. Sagittaria sagittifolia polysaccharide (SSP) extract, a key component of Sagittaria sagittifolia L., exhibits anti-oxidant and anti-apoptotic effects with potential applications in ARC.
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