Bioinformatics Analysis Reveals MicroRNA-193a-3p Regulates ACTG2 to Control Phenotype Switch in Human Vascular Smooth Muscle Cells
Authors: Zhicheng Zhu
Yong Wang
Weitie Wang
Dan Li
Tiance Wang
Bo Li
Kexiang Liu
Hulin Piao
Journal: Frontiers in Genetics (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: aortic dissection; cardiovascular; mRNA; miRNA; vascular disease.
Affiliations: Department of Cardiovascular Surgery of the Second Hospital of Jilin University, The Second Hospital of Jilin University, Changchun, China.

Abstract:  Aortic dissection (AD) is among the most fatal cardiovascular diseases. However, the pathogenesis of AD remains poorly understood. This study aims to integrate the microRNAs (miRNA) and mRNA profiles and use bioinformatics analyses with techniques in molecular biology to delineate the potential mechanisms involved in the development of AD. We used the human miRNA and mRNA microarray datasets GSE98770, GSE52093, and GEO2R, Venn diagram analysis, gene ontology, and protein-protein interaction networks to identify target miRNAs and mRNAs involved in AD. RNA interference, western blotting, and luciferase reporter assays were performed to validate the candidate miRNAs and mRNAs in AD tissues and human vascular smooth muscle cells (VSMCs). Furthermore, we studied vascular smooth muscle contraction in AD. In silico analyses revealed that miR-193a-3p and ACTG2 were key players in the pathogenesis of AD. miR-193a-3p was upregulated in the AD tissues. We also found that biomarkers for the contractile phenotype in VSMCs were downregulated in AD tissues. Overexpression and depletion of miR-193a-3p enhanced and suppressed VSMC proliferation and migration, respectively. Dual luciferase reporter assays confirmed that ACTG2 was a target of miR-193a-3p. ACTG2 was also downregulated in human AD tissues and VMSCs overexpressing miR-193a-3p. Taken together, miR-193a-3p may be a novel regulator of phenotypic switching in VSMCs and the miR-193a-3p/ACTG2 axis may serve as a promising diagnostic biomarker and therapeutic candidate for AD. 

Retracted: No

PubPeer comments:
 2021 retraction. https: journals.plos.org plosone article?id=10.1371 journal.pone.0261919 Following the publication of this article [1], the editorial team has become aware of a highly similar manuscript that was previously submitted for consideration in PLOS ONE and subsequently withdrawn by the authors. Despite high similarity between the two bodies of work, the authors and affiliations listed on the withdrawn submission are different from the authors and affiliations listed on the published article. The authors have not responded to communications regarding the similarity between the submissions and the authorship concerns. It remains unclear who conducted the research described in this article [1] and whether the listed authors met authorship criteria of the PLOS ONE policy. In light of the unresolved concerns the PLOS ONE Editors retract this article. The authors either did not respond directly or could not be reached. Reference 1.Fu D, Cong X, Ma Y, Cai H, Cai M, Li D, et al. (2013) Genetic Polymorphism of Glucokinase on the Risk of Type 2 Diabetes and Impaired Glucose Regulation: Evidence Based on 298, 468 Subjects. PLoS ONE 8(2): e55727. , 
 I am the first author of this paper. We are sorry that we did not communicate and reply to the magazine in time. Maybe the editor s email was omitted by the author because it was treated as spam or advertising email. We published this paper in 2013. Someones we do not know plagiarized our articles and data and submit to PlosOne in 2021. The editor of the magazine found the plagiarism and suspend the submission. However, the magazine withdrew our article because we didn t reply to the editor s email in time. We strongly urge the magazine to reveal the names and units of the plagiarists and cancel the withdrawal of our article. ,