Open Access

miR‑23a‑3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl‑2 in an in vitro model of cataracts

  • Authors:
    • Pengxiang Yao
    • Jian Jiang
    • Xiaoping Ma
    • Zhenzhong Chen
    • Yufang Hong
    • Yang Wu
  • View Affiliations

  • Published online on: February 26, 2021     https://doi.org/10.3892/etm.2021.9853
  • Article Number: 436
  • Copyright: © Yao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cataracts account for ~50% of the cases of blindness in individuals worldwide. The apoptosis of lens epithelial cells (LECs) occurs during the formation of cataracts, which is a non‑congenital condition. Numerous microRNAs (miRs) have been reported to regulate apoptosis in LECs. For instance, miR‑23a expression levels were shown to be upregulated in cataractous lenses; however, the function of miR‑23a in cataracts remains undetermined. To establish an in vitro model of cataracts, human LECs, HLE‑B3 cells, were induced with 200 µmol/l H2O2 for 24 h. HLE‑B3 cells were transfected with the miR‑negative control (NC) mimic, miR‑23a‑3p mimic, miR‑NC inhibitor, miR‑23a‑3p inhibitor, small interfering RNA (siRNA) targeting BCL2 (siRNA‑BCL2) and siRNA‑NC. The expression levels of miR‑23a‑3p were detected using reverse transcription‑quantitative PCR. The interaction between miR‑23a‑3p and the 3'‑untranslated region (UTR) of the target mRNA BCL2 was predicted by TargetScan 7.1, and further validated using a dual luciferase reporter assay. The BCL2 protein expression levels were analyzed using western blotting, cell proliferation was determined using a CCK‑8 assay and the levels of cell apoptosis were analyzed using flow cytometric analysis. The results of the present study revealed that the expression levels of miR‑23a‑3p were significantly upregulated, while the expression levels of BCL2 were significantly downregulated in H2O2‑induced HLE‑B3 cells compared to untreated control cells. BCL2 was shown to be a target of miR‑23a‑3p. The miR‑23a‑3p inhibitor subsequently attenuated H2O2‑induced apoptosis and increased the proliferation of HLE‑B3 cells, which was partially reversed by siRNA‑BCL2. In conclusion, the findings of the current study suggested that the inhibition of miR‑23a‑3p may attenuate H2O2‑induced cataract formation by targeting BCL2, thus providing a novel therapeutic target for the treatment of patients with cataracts in the clinic.
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May-2021
Volume 21 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Yao P, Jiang J, Ma X, Chen Z, Hong Y and Wu Y: miR‑23a‑3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl‑2 in an <em>in vitro</em> model of cataracts. Exp Ther Med 21: 436, 2021
APA
Yao, P., Jiang, J., Ma, X., Chen, Z., Hong, Y., & Wu, Y. (2021). miR‑23a‑3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl‑2 in an <em>in vitro</em> model of cataracts. Experimental and Therapeutic Medicine, 21, 436. https://doi.org/10.3892/etm.2021.9853
MLA
Yao, P., Jiang, J., Ma, X., Chen, Z., Hong, Y., Wu, Y."miR‑23a‑3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl‑2 in an <em>in vitro</em> model of cataracts". Experimental and Therapeutic Medicine 21.5 (2021): 436.
Chicago
Yao, P., Jiang, J., Ma, X., Chen, Z., Hong, Y., Wu, Y."miR‑23a‑3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl‑2 in an <em>in vitro</em> model of cataracts". Experimental and Therapeutic Medicine 21, no. 5 (2021): 436. https://doi.org/10.3892/etm.2021.9853