Aberrant expression of COL4A1 in age-related cataract and its effect on cell proliferation, apoptosis and gene expression changes
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Peng Li. Department of Ophthalmology, Xijing 986 Hospital Department, Fourth Military Medical University, Xi'an 710054, Shaanxi Province, China. drlipeng@126.com

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Supported by Supporting Fund Project of Shaanxi Provincial Department of Science and Technology Agency Project (No.2022SF-502); Special Scientific Research Program of Education Department of Shaanxi Provincial Government (No.21JK0891); Young Talent Lifting Project of Xi'an Science and Technology Association (No.095920221365); Innovation and Entrepreneurship Training Program for College students of Xi'an Medical University (No.121521113).

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    Abstract:

    AIM: To evaluate the regulation of the aberrant expression of collagen type IV alpha 1 chain (COL4A1) in the development of age-related cataract (ARC). METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot analysis were employed to evaluate the expression of COL4A1 in ARC patients and healthy controls. The proliferation, apoptosis, cell cycle and epithelial-mesenchymal transition (EMT) of human lens epithelial cell (HLE-B3) were further analyzed under the condition of COL4A1 gene silence. Alteration of gene expression at mRNA level after knockdown COL4A1 were also evaluated by qRT-PCR on HLE-B3 cells. RESULTS: The aberrant expression of COL4A1 was identified a clinically associated with the ARC. Silencing of COL4A1 promoted the apoptosis and inhibited the proliferation of HLE-B3 by blocking the cell cycle. Moreover, COL4A1 gene silence didn't affect the cytoskeleton of HLE-B3 but down-regulated the Collagen type IV Alpha 2 Chain (COL4A2), paired box 6 (PAX6), procollagen-lysine 2-oxoglutarate 5-dioxygenases 1 (PLOD1) and procollagen-lysine 2-oxoglutarate 5-dioxygenases 2 (PLOD2) expression levels in HLE-B3 cells. Silencing the COL4A1 gene induced EMT of the HLE-B3 cells by promoting the transforming growth factor beta (TGF-β) expression. CONCLUSION: Silencing of COL4A1 induces S-phase arrest, also inhibits the proliferation and enhance HLE-B3 apoptosis and EMT, and down-regulates the expression of COL4A2, PAX6, PLOD1 and PLOD2. Thus, the expression alteration of COL4A1 may play a critical role in the pathogenesis of ARC.

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Dan Zhu, Peng Li, Li Wang, et al. Aberrant expression of COL4A1 in age-related cataract and its effect on cell proliferation, apoptosis and gene expression changes. Int J Ophthalmol, 2023,16(3):333-341

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Publication History
  • Received:March 21,2022
  • Revised:January 12,2023
  • Adopted:
  • Online: March 02,2023
  • Published: