Search Results (2)

Background/Objectives: Evaluation of stem cell, keratin, retinoic acid metabolism markers and non-coding micro-RNAs (miRNAs) in conjunctival and corneal samples of patients with epithelial basal membrane dystrophy (EBMD), Salzmann nodular degeneration (SND), pterygium and congenital aniridia (CA), to detect similarities and differences in their pathogenesis. Methods: Impression cytology (IC) samples and corneal epithelial samples (CEs) of patients with EBMD, SND, pterygium, congenital aniridia, and healthy control subjects have been analyzed. The IC samples were subjected to qPCR, and the epithelial samples were subjected to qPCR and WB. Limbal epithelial stem cell markers, keratins, retinoic acid metabolism markers, and miRNAs were analyzed. Results: In conjunctival IC samples, PAX6 mRNA expression was significantly lower in EBMD, SND, pterygium, and CA compared to healthy controls (p ≤ 0.02). KRT13 mRNA expression was significantly higher in EBMD, SND, and pterygium (p ≤ 0.018), and FABP5 was increased in pterygium samples (p = 0.007). MiRNA-138-5p was significantly higher in aniridia samples than in normal controls (p = 0.037). In corneal epithelial samples, PAX6 protein, DSG1 mRNA and protein, miRNA-138-5p, and miR-204-5p expression were significantly lower in EBMD, SND, and pterygium samples than in controls (p ≤ 0.02). ALDHA1 mRNA expression was significantly lower (p < 0.0001), and FABP5 mRNA expression was significantly higher (p = 0.014) in pterygium samples than in controls. Conclusions: PAX6, DSG1, miR-138-5p, and miR-204-5p expression is decreased in the corneal epithelium of epithelial basal membrane dystrophy, Salzmann nodular degeneration, and pterygium subjects. In addition, there is a dysregulation of markers of the retinoic acid signaling pathway, such as ADH1A1 and FABP5, in the corneal epithelium of pterygium subjects. These changes may offer therapeutic targets in the treatment of these ocular surface diseases. Full article

Matrix metalloproteinases (MMPs) are a group of proteolytic enzymes which are members of the zinc endopeptidase family. They have the ability to degrade extracellular matrix elements, allowing for the release of binding molecules and cell migration. Although metalloproteinases regulate numerous physiological processes within the cornea, overexpression of metalloproteinase genes and an imbalance between the levels of metalloproteinases and their inhibitors can contribute to the inhibition of repair processes, the development of inflammation and excessive cellular proliferation. The involvement of MMPs in the pathogenesis of dystrophic corneal diseases needs clarification. Our analyses focus on the involvement of individual metalloproteinases in the pathogenesis of recurrent corneal erosions and highlight their impact on the development of corneal epithelial basement membrane dystrophy (EBMD). We hypothesize that abnormalities observed in patients with EBMD may result from the accumulation and activation of metalloproteinases in the basal layers of the corneal epithelium, leading to basement membrane degradation. A barrier formed from degradation materials inhibits the normal migration of epithelial cells to the superficial layers, which contributes to the development of the aforementioned lesions. This hypothesis seems to be lent support by the elevated concentrations of metalloproteinases in the corneal epithelium of these patients found in our previous studies on the relationships between MMPs and recurrent corneal erosions. Full article