Abstract
Background
Ischemic stroke has been a public concern, while its pathogenesis is not fully understood.
Increasing evidence suggests that circular RNAs (circRNAs) are involved in this disorder.
The purpose of this study was to explore the role of circ_0101874 in ischemic stroke.
Methods
The in vivo model of ischemic stroke was established in mice with middle cerebral artery occlusion
(MCAO) treatment. The in vitro model of ischemic stroke was established in SK-N-SH cells with oxygen-glucose deprivation
(OGD) treatment. The expression of circ_0101874, miR-335-5p and phosphodiesterase
4D (PDE4D) mRNA was measured by quantitative real-time PCR (qPCR). The release of
inflammatory factors was checked by ELISA. Cell viability, cell proliferation and
cell apoptosis were detected using CCK-8 assay, EdU assay and flow cytometry assay,
respectively. The protein levels of cyclinD1, cleaved-caspase-3 and PDE4D were detected
by western blot. The interaction between miR-335-5p and circ_0101874 or PDE4D was
validated by dual-luciferase reporter assay and RIP assay.
Results
Circ_0101874 was highly expressed in MCAO animal models and OGD-induced SK-N-SH cells.
Circ_0101874 knockdown suppressed OGD-enhanced inflammation, cell apoptosis and oxidative
stress and promoted OGD-inhibited cell viability and cell proliferation in SK-N-SH
cells. Circ_0101874 directly bound to miR-335-5p, and miR-335-5p inhibition reversed
the effects of circ_0101874 knockdown. PDE4D was a target gene of miR-335-5p, and
PDE4D overexpression recovered OGD-promoted SK-N-SH cell injuries that were blocked
by miR-335-5p enrichment. Circ_0101874 bound to miR-335-5p to enhance the expression
of PDE4D.
Conclusion
Circ_0101874 knockdown alleviated OGD-induced neuronal cell injury by suppressing
PDE4D via regulating miR-335-5p.
Keywords
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Article info
Publication history
Published online: October 14, 2022
Accepted:
September 29,
2022
Received in revised form:
September 26,
2022
Received:
July 15,
2022
Identification
DOI: https://doi.org/10.1016/j.jstrokecerebrovasdis.2022.106817
Copyright
© 2022 Elsevier Inc. All rights reserved.
