Delivery of miR-654-5p via SonoVue Microbubble Ultrasound Inhibits Proliferation, Migration, and Invasion of Vascular Smooth Muscle Cells and Arterial Thrombosis and Stenosis through Targeting TCF21

Abstract

Background. Abnormal proliferation of vascular smooth muscle cells (VSMCs) is an important cause of vascular stenosis. The study explored the mechanism of inhibition of vascular stenosis through the molecular mechanism of smooth muscle cell phenotype transformation. Methods. Coronary heart disease-related genes were screened by bioinformatics, and the target genes of miR-654-5p were predicted by dual-luciferase method and immunofluorescence method. miR-654-5p mimic stimulation and transfection of TCF21 and MTAP into cells. SonoVue microbubble sonication was used to deliver miR-654-5p into cells. Cell proliferation, migration, and invasion were detected by CCK-8, wound scratch, and Transwell. HE and IHC staining were performed to study the effect of miR-654-5p delivery via SonoVue microbubble ultrasound on vessel stenosis in a model of arterial injury. Gene expression was determined by qRT-PCR and WB. Results. TCF21 and MTAP were predicted as the target genes of miR-654-5p. Cytokines induced smooth muscle cell proliferation, migration, and invasion and promoted miR-654-5p downregulation; noticeably, downregulated miR-654-5p was positively associated with the cell proliferation and migration. Overexpression of TCF21 promoted proliferation, invasion, and migration, and mimic reversed such effects. miR-654-5p overexpression delivered by SonoVue microbubble ultrasound inhibited proliferation, migration, and invasion of cells. Moreover, in arterial injury model, we found that SonoVue microbubble ultrasound transmitted miR-654-5p into the arterial wall to inhibit arterial thrombosis and stenosis, while TCF21 was inhibited. Conclusion. Ultrasound delivery of miR-654-5p via SonoVue microbubbles was able to inhibit arterial thrombosis and stenosis by targeting TCF21.

Pyroptosis and mitochondrial function participated in miR-654-3p-protected against myocardial infarction

“…miR-654-3p is also participated in lncRNA ZDAS1-modulated cholesterol efflux in atherosclerosis [ 36 ]. Delivery of miR-654-5p via SonoVue microbubble ultrasound inhibits proliferation, migration, and invasion of vascular smooth muscle cells and arterial thrombosis and stenosis [ 37 ]. Our present data found that miR-654-3p is downregulated in response to MI and participated in the MI regulation.…”

Transcription Factor 21: A Transcription Factor That Plays an Important Role in Cardiovascular Disease

“…Recent studies have reported that miR-654-5p is an important gene that regulates VSMC phenotypic transformation. It can inhibit the expression of TCF21 and cell proliferation, invasion, and metastasis [4]. That is, it can inhibit arterial thrombosis and stenosis by targeting TCF21.…”

“…Aberrant proliferation of vascular smooth muscle cells (VSMCs) in AS promotes plaque formation, but VSMCs in advanced plaques are beneficial by preventing fibrous cap rupture [3]. Recent studies have found that decreased expression of the transcription factor 21 (TCF21) can inhibit the proliferation and migration of VSMCs and inhibit arterial thrombosis and lumen stenosis [4].…”

Retracted: Delivery of miR-654-5p via SonoVue Microbubble Ultrasound Inhibits Proliferation, Migration, and Invasion of Vascular Smooth Muscle Cells and Arterial Thrombosis and Stenosis through Targeting TCF21

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Manipulated or compromised peer review …”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”