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MicroRNA-124 facilitates lens epithelial cell apoptosis by inhibiting SPRY2 and MMP-2.

Authors
  • Liu, Yan1
  • Li, Shuting1
  • Liu, Yao1
  • Lv, Xujing1
  • Zhou, Qing2
  • 1 Department of Ophthalmology, The First People's Hospital of Changzhou, Changzhou, Jiangsu 223000, P.R. China. , (China)
  • 2 Department of Third Institute of Clinical Medicine, Soochow University, Suzhou, Jiangsu 215006, P.R. China. , (China)
Type
Published Article
Journal
Molecular Medicine Reports
Publisher
Spandidos Publications
Publication Date
May 01, 2021
Volume
23
Issue
5
Identifiers
DOI: 10.3892/mmr.2021.12020
PMID: 33760112
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Age-related cataract (ARC) is the primary cause of blindness worldwide. Abnormal expression of microRNAs (miRNAs/miRs) has been reported to be associated with multiple diseases, including ARC. However, the potential role of miR-124 in ARC remains unclear. The present study used the human lens epithelial cell line, SRA01/04, to investigate the potential role of miR-124 in ARC. Reverse transcription-quantitative PCR analysis was performed to detect the expression levels of miR-124, protein sprouty homolog 2 (SPRY2) and matrix metalloproteinase-2 (MMP-2) in ARC tissues, while western blotting was performed to detect the protein levels of SPRY2 and MMP-2. Cell viability and apoptosis of SRA01/04 cells were assessed via Cell Counting Kit-8 and TUNEL assays, respectively. The interaction between miR-124 and SPRY2 or MMP-2 was confirmed via the dual-luciferase reporter and RNA immunoprecipitation assays. The results of the present study demonstrated that miR-124 expression was significantly upregulated in ARC tissues, and knockdown of miR-124 increased SRA01/04 cell viability and suppressed apoptosis. In addition, SPRY2 and MMP-2 expression was decreased in ARC tissues, and were demonstrated to directly bind to miR-124. Overexpression of SPRY2 or MMP-2 increased SRA01/04 cell viability and repressed apoptosis, the effects of which were reversed following overexpression of miR-124. Taken together, these results suggested that miR-124 facilitates lens epithelial cell apoptosis by modulating SPRY2 or MMP-2 expression, providing a novel treatment approach for ARC.

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