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Hsa_circRNA_102541 regulates the development of atherosclerosis by targeting miR-296-5p/PLK1 pathway

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Abstract

Background:

Cardiovascular disorders pose great threat to public health. As a common type of cardiovascular disease, atherosclerosis is characterized by high morbidity and mortality/recurrence rate. However, the pathogenesis of atherosclerosis is complex and not fully understood. The aim of this study was to investigate the influences of hsa_circRNA_102541 (circ_102541) on proliferation and apoptosis of HUVEC cells and to identify the underlying mechanisms.

Methods:

RT-PCR was used to determine the expression levels of circ_102541, miR-296-5p, and PLK1 in atherosclerosis and healthy blood samples. Following the transfection with sh-circ_102541, LV-circ_102541, miR-296-5p mimics, miR-296-5p inhibitors, and si-PLK1, cell proliferation was evaluated using CCK8 assay; cell apoptosis was determined by flow cytometry; dual luciferase assay was performed to examine the interaction between abovementioned molecules. The levels of associated markers including PCNA and caspase-3 were assessed by western blotting and RT-qPCR.

Results:

The expression of circRNA_102541 and PLK1 were significantly elevated in atherosclerosis specimens, where the level of miR-296-5p was reduced. Furthermore, circRNA_102541 could bind miR-296-5p and subsequently target PLK1. Following treatment with sh-circRNA_102541 or miR-296-5p mimics, proliferative ability and levels of PCNA were remarkably reduced in HUVEC cells, while apoptosis was significantly enhanced. Co-transfection with miR-296-5p mimics abrogated the effects induced by the overexpressed circ_102541. Additionally, treatment with si-PLK1 attenuated the biological behavior changes caused by miR-296-5p inhibitors in HUVEC cells. Moreover, transfection with LV-PLK1 reversed the effects triggered by miR-296-5p mimics.

Conclusion:

Taken together, circRNA_102541 was upregulated in atherosclerosis, and knockdown of circRNA_102541 suppressed cell proliferation while promoted apoptosis of HUVEC cells via miR-296-5p/PLK1. This novel pathway may serve essential roles on the development of atherosclerosis, and circRNA_102541 could be a promising therapeutic candidate for the treatment of atherosclerosis.

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Data availability

The datasets generated or analyzed during the present study are included in this published article.

Abbreviations

HUVEC:

Human umbilical vein endothelial cells

PCNA:

Proliferating cell nuclear antigen

PLK1:

Polo-like kinase 1

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Authors and Affiliations

  1. Department of Cardiology, the First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, 121001, People’s Republic of China

    Na Du

  2. Liaoning Jinqiu Hospital, Shenyang, Liaoning, 110015, People’s Republic of China

    Mingjin Li

  3. Department of Dermatology, the First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, 121001, People’s Republic of China

    Dan Yang

Authors
  1. Na Du
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  2. Mingjin Li
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  3. Dan Yang
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Contributions

DY initiated the present study. ND, ML, and DY carried out the experiments and data analysis. All the authors drafted the manuscript and approved the final version.

Corresponding author

Correspondence to Dan Yang.

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Ethics approval

The present study was approved by the Ethics Committee of the First Affiliated Hospital of Jinzhou Medical University (Jinzhou, China).

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Written informed consents were signed by our patients.

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The authors declare no competing interests.

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Du, N., Li, M. & Yang, D. Hsa_circRNA_102541 regulates the development of atherosclerosis by targeting miR-296-5p/PLK1 pathway. Ir J Med Sci 191, 1153–1159 (2022). https://doi.org/10.1007/s11845-021-02708-x

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  • DOI: https://doi.org/10.1007/s11845-021-02708-x

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