Inhibition of miR-29a-3p Alleviates Apoptosis of Lens Epithelial Cells via Upregulation of CAND1

Curr Eye Res. 2024 Apr;49(4):391-400. doi: 10.1080/02713683.2023.2293457. Epub 2023 Dec 14.

Abstract

Purpose: Accumulated evidence has shown that microRNAs (miRNAs) are closely related to the pathogenesis and progression of senile cataracts. Here we investigate the effect of miR-29a-3p in cataractogenesis and determined the potential molecular mechanism involved.

Methods: In this study, we constructed a selenite cataract model in rats and obtained the miRNAs related to cataracts by whole transcriptome sequencing. To investigate the effect and mechanism of miR-29a-3p on cataracts, we performed several in vivo and in vitro experiments, including CCK8 assay, flow cytometry, luciferase reporter assay, Edu assay, and western blot analysis.

Result: Sequencing data showed downregulation of miR-29a-3p in rats with selenite cataracts. Down-regulation of miR-29a-3p could promote lens epithelial cells (SRA01/04) proliferation and inhibit cell apoptosis, and miR-29a-3p silence could inhibit the development of cataracts. Additionally, CAND1 was a direct target gene for miR-29a-3p.

Conclusion: These data demonstrate that miR-29a-3p inhibits apoptosis of lens epithelial cells by regulating CAND1, which may be a potential target for senile cataracts.

Keywords: CAND1; apoptosis; lens epithelial cells; miR-29a-3p; senile cataract.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Cataract* / genetics
  • Cataract* / pathology
  • Cell Proliferation
  • Epithelial Cells / pathology
  • MicroRNAs* / genetics
  • Rats
  • Selenious Acid
  • Up-Regulation

Substances

  • MicroRNAs
  • Selenious Acid