The Current State of MicroRNAs as Restenosis Biomarkers

Varela, Nelson; Lanas, Fernando; Salazar, Luis A.; Zambrano, Tomás

doi:10.3389/fgene.2019.01247

Cited by 11 publications

(12 citation statements)

References 93 publications

(102 reference statements)

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“…A number of studies have explored the role of miRNAs in atherosclerosis and stenosis ( 30 – 32 ). Several circulating miRNAs are considered as biomarkers for restenosis ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Potential Target miR-455 Delaying Arterial Stenosis Progression Through PTEN

Lin

Wang

et al. 2021

Front. Cardiovasc. Med.

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Background: Vascular smooth muscle cells (VSMC) underwent phenotypic switching upon stimulation signals, and this is the prerequisite for their proliferation and migration. Previous work revealed that miR-455 may be involved in vascular stenosis. Thus, this study aimed to explore potential targets and mechanisms underlying the dynamics of miR-455 in vascular stenosis.Methods: miR-455 and PTEN expression levels were studied in normal and stenosis tissue, as well as in VSMC in proliferation model. Manipulating miR-455 expression levels was achieved by transfection of either miR-455 mimic or inhibitor, and its effect on cell proliferation was studied by CCK-8 assay. Its effect on gene expression was studied by RT-qPCR and western blot. The expression regulation mechanism was studied by luciferase reporter system. Finally, the effect of miR-455 on regulating vascular stenosis was studied using a rat balloon-injured carotid artery stenosis model.Results: High expression levels of miR-455 were detected in both stenosis arterial tissues and VSMC proliferation models. In contrast, the expression levels of PTEN were downregulated in these systems. miR-455 transfected VSMC showed higher levels of proliferation and decreased levels of PTEN. Potential binding sites between miR-455 and PTEN 3′UTR were predicted and confirmed. NF-kB p65 was found to bind directly on miR-455 promoter region and regulate its transcription. The progression of arterial stenosis could be delayed by introducing miR-455 antagomir.Conclusions: The p65/miR-455/PTEN signaling pathway plays a crucial role in regulating VSMC proliferation and vascular stenosis. This indicated that miR-455 is a novel target that would help improve treatment outcomes in patients suffering from vascular stenosis.

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“…A number of studies have explored the role of miRNAs in atherosclerosis and stenosis ( 30 – 32 ). Several circulating miRNAs are considered as biomarkers for restenosis ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Potential Target miR-455 Delaying Arterial Stenosis Progression Through PTEN

Lin

Wang

et al. 2021

Front. Cardiovasc. Med.

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“…Nevertheless, the application of BMSs is limited by the high rate of in-stent restenosis (ISR), which is mainly caused by the generation of a neointima. 6 , 7 The emergence of drug-eluting stents (DESs) (especially second-generation) and drug-coated balloons (DCBs) has further reduced the incidence of restenosis by <10%. 8 However, current DESs cannot effectively repress the proliferation and migration of vascular smooth muscle cells (VSMCs) and cannot induce adequate re-endothelialization within the vasculature, which increases the risk of restenosis.…”

Section: Main Textmentioning

confidence: 99%

“… 17 These cytokines regulate the phenotypic transformation of VSMCs and change from contractile to synthetic, resulting in proliferation and migration, following which they enter the cell cycle and migrate to the intimal and extracellular matrix (ECM) to then form neointima. 7 , 18 …”

Section: Main Textmentioning

confidence: 99%

Targeting the epigenome in in-stent restenosis: from mechanisms to therapy

Yang

Guo

et al. 2021

Molecular Therapy - Nucleic Acids

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Coronary artery disease (CAD) is one of the most common causes of death worldwide. The introduction of percutaneous revascularization has revolutionized the therapy of patients with CAD. Despite the advent of drug-eluting stents, restenosis remains the main challenge in treating patients with CAD. In-stent restenosis (ISR) indicates the reduction in lumen diameter after percutaneous coronary intervention, in which the vessel’s lumen re-narrowing is attributed to the aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) and dysregulation of endothelial cells (ECs). Increasing evidence has demonstrated that epigenetics is involved in the occurrence and progression of ISR. In this review, we provide the latest and comprehensive analysis of three separate but related epigenetic mechanisms regulating ISR, namely, DNA methylation, histone modification, and non-coding RNAs. Initially, we discuss the mechanism of restenosis. Furthermore, we discuss the biological mechanism underlying the diverse epigenetic modifications modulating gene expression and functions of VSMCs, as well as ECs in ISR. Finally, we discuss potential therapeutic targets of the small molecule inhibitors of cardiovascular epigenetic factors. A more detailed understanding of epigenetic regulation is essential for elucidating this complex biological process, which will assist in developing and improving ISR therapy.

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“…Nevertheless, an ineluctable clinical problem of this therapy is in-stent restenosis (ISR), which occurs in approximately 20% of CHD patients with drug-eluting stents implantation [1]. It is generally believed that ISR can be brie y divided into 3 phases including a damage to the endothelium, the migration and proliferation of vascular smooth muscle cells (VSMCs) and the late remodeling phase [2]. Despite many approaches were used for clarifying the mechanism as well as the prevention of ISR, however, it is still a tricky problem that has not been completely solved [3].…”

Section: Introductionmentioning

confidence: 99%

“…In view of these, cell therapy with EPCs may offer a promising strategy for accelerating reendothelialization and maintaining endothelial integrity in ISR [9]. Importantly, the microenvironment in ISR is essential for EPCs fate and function, especially in ammation, which is closely followed with endothelial injury, including platelet activation and recruitment of circulating leukocytes, releasing cytokines and growth factors [2].…”

Section: Introductionmentioning

confidence: 99%

Endothelial progenitor cells overexpressed with omentin-1 enhance the inhibition of neointimal hyperplasia via anti-inflammation

Xiang

Zhou

et al. 2021

Preprint

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Background Endothelial progenitor cells (EPCs) play an important role in vascular repair. However, the functions of EPCs are obviously weakened in inflammatory microenvironment during restenosis. Therefore, we investigated whether omentin-1, an anti-inflammatory factor, can reduce neointima formation after carotid artery injury (CAI) in rats via improving EPCs functions damaged by inflammation and the underlying mechanisms. Methods Rats bone marrow-derived EPCs were isolated and cultured. EPCs were transfected with adenovirus vectors expressing human omentin-1 or green fluorescent protein (GFP). Rats received 2×106 EPCs with expressing omentin-1 or GFP by tail vein injection directly after CAI and again 24 h later. Hematoxylin-eosin staining and immunohistochemistry were used for analyzing neointimal hyperplasia. Besides, EPCs were treated with omentin-1 and tumor necrosis factor-α (TNF-α) in order to explore the underlying mechanism. Results Omentin-1 could significantly promote EPCs proliferation and tube formation, as well as inhibit apoptosis. EPCs overexpressed with omentin-1 using adenovirus vectors could extremely reduce the neointimal hyperplasia after CAI in rats. Besides, TNF-α could notably induce EPCs dysfunction including reduced proliferation, migration tube formation and increased apoptosis, which can be remarkably attenuated by omentin-1 via inhibiting of p38/CREB pathway. Besides, p38 agonist (anisomycin) could significantly reverse the protective effects of omentin-1 which attenuated the injury effects of TNF-α on EPCs. Conclusions EPCs overexpressed with omentin-1 can significantly reduce neointima formation after arterial injury by enhancing the functions of EPCs via inhibiting the p38/CREB pathway. Our results indicate that gene modified EPCs with omentin-1 may be an alternative strategy for the treatment of restenosis.

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The Current State of MicroRNAs as Restenosis Biomarkers

Cited by 11 publications

References 93 publications

Potential Target miR-455 Delaying Arterial Stenosis Progression Through PTEN

Potential Target miR-455 Delaying Arterial Stenosis Progression Through PTEN

Targeting the epigenome in in-stent restenosis: from mechanisms to therapy

Endothelial progenitor cells overexpressed with omentin-1 enhance the inhibition of neointimal hyperplasia via anti-inflammation

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