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Circ_HIPK3 Inhibits H2O2-Induced Lens Epithelial Cell Injury in Age-Related Cataract Depending on the Regulation of miR-495-3p/HDAC4 Pathway

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Abstract

Age-related cataract (ARC) is one of the most common chronic diseases. Circular RNA (circ)_HIPK3 is reported to be involved in the advancement of ARC, but its molecular mechanism has not been clarified. Our study provides a new perspective on the clinical treatment of ARC. Our data showed that the expression levels of circ_HIPK3 and histone deacetylase 4 (HDAC4) were downregulated, while microRNA (miR)-495-3p level was increased in ARC tissues and H2O2-induced SRA01/04 cells. Functional experiments showed that circ_HIPK3 and HDAC4 overexpression could inhibit H2O2-induced lens epithelial cell apoptosis and fibrosis. In terms of mechanism, we found that circ_HIPK3 could sponge miR-495-3p, miR-495-3p could target HDAC4. Besides, we confirmed that circ_HIPK3 sponged miR-495-3p to positively regulate HDAC4. Additionally, miR-495-3p overexpression or HDAC4 knockdown reversed the inhibition effect of circ_HIPK3 on H2O2-induced lens epithelial cell injury. In conclusion, our data showed that circ_HIPK3 suppressed H2O2-induced lens epithelial cell injury by regulating miR-495-3p/HDAC4 axis.

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Data Availability

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

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Correspondence to Wenqian Wang.

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The design of this protocol follows the tenets of the Declaration of Helsinki, approved by the Ethics Committee of Jingmen No.1 people’s Hospital.

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Chen, S., Wang, M., Jian, R. et al. Circ_HIPK3 Inhibits H2O2-Induced Lens Epithelial Cell Injury in Age-Related Cataract Depending on the Regulation of miR-495-3p/HDAC4 Pathway. Biochem Genet 61, 565–577 (2023). https://doi.org/10.1007/s10528-022-10266-9

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