The following is a summary of “IL-1β induced down-regulation of miR-146a-5p promoted pyroptosis and apoptosis of corneal epithelial cell in dry eye disease through targeting STAT3,” published in the March 2024 issue of Ophthalmology by Li et al.
Researchers conducted a retrospective study exploring how IL-1β influences dry eye disease (DED) progression through its effects on pyroptosis and apoptosis in corneal epithelial cells (CECs).
They employed 400 milliosmoles per kilogram (mOsM) solutions to establish the DED model (hCECs-DED). IL-1β mRNA and miR-146a-5p in CECs were measured using RT-qPCR. STAT3, GSDMD, NLRP3, and Caspase-1 levels were assessed via Western blotting. Cell viability was examined with the cell counting kit-8 assay. Flow cytometry was utilized to detect apoptosis. ELISAs were conducted to determine levels of IL-18, IL-33, and LDH. Targeting relationships were detected using the luciferase test.
The results showed that following treatment with a 400 mOsM solution, a decrease in cell viability and increased apoptosis was observed. In hCECs-DED compared to hCECs, IL-1β levels were higher, and miR-146a-5p levels were lower. Additionally, GSDMD, NLRP3, Caspase-1, IL-18, IL-33, and LDH were significantly elevated in hCECs-DED compared to hCECs, whereas IL-1β silencing reversed this effect. Furthermore, IL-1β negatively regulated miR-146a-5p, and miR-146a-5p mimics alleviated the inhibition of pyroptosis and apoptosis in hCECs-DED caused by IL-1β silencing. Concurrently, miR-146a-5p decreased STAT3 levels in hCECs.
Investigators concluded that high levels of IL-1β in DED trigger cell death in CECs by reducing miR-146a-5p and inhibiting STAT3.
Source: bmcophthalmol.biomedcentral.com/articles/10.1186/s12886-024-03396-8