DIABETOLOGY / RESEARCH PAPER
MiR-28-3p regulates high glucose-induced endothelial dysfunction by targeting CXXC5
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1
Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China., China
2
Department of Vascular Surgery, Hangzhou Third People’s Hospital, Hangzhou, China., China
3
Department of Vascular Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China., China
Submission date: 2023-05-29
Final revision date: 2023-07-30
Acceptance date: 2023-08-14
Online publication date: 2023-08-17
Corresponding author
Chenyang Qiu
Department of Vascular Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China., No.79 Qingchun Road, 310003, Hangzhou, China
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ABSTRACT
Introduction:
Introduction: Data from the CEO database shows microRNA (miR) -28-3p levels are elevated in diabetic patients. Nevertheless, the role of miR-28-3p in peripheral artery disease with diabetes have not been investigated.
Material and methods:
The level of miR-28-3p, CXXC5, CXXC-type zinc finger protein 5, and CXXC5’s downstream molecules as well as endothelial function were investigated. Dual luciferase analyses were used to confirm the binding site of miR-28-3p and CXXC5.
Results:
Results: Under high-glucose condition, miR-28-3p expression is increased whereas CXXC5 expression is downregulated. Overexpression of miR-28-3p increased cell apoptosis and inhibited cell proliferation, migration, and vessel formation, whilst inhibiting its expression had the opposite effect. The overexpression and inhibition of miR-28-3p could also influence both the mRNA and protein levels of CXXC5 and its known downstream molecules. Analysis of bioinformatics data revealed a potential binding site for miR-28-3p and CXXC5. Dual luciferase analyses demonstrated that miR-28-3p suppressed CXXC5 expression by targeting the 3'-untranslated region (3'-UTR) of CXXC5. Following that, we overexpressed both miR-28-3p and CXXC5. The level of CXXC5 and its known downstream signaling molecules decreased with miR-28-3p overexpression alone. As anticipated, co-overexpression of miR-28-3p and CXXC5 partially reversed the effect of miR-28-3p mimics.
Conclusions:
Conclusion: These findings indicated that miR-28-3p regulated high glucose-induced endothelial dysfunction by targeting CXXC5.