miR-128-3p Is a Novel Regulator of Vascular Smooth Muscle Cell Phenotypic Switch and Vascular Diseases

Farina, Floriana Maria; Hall, Ignacio Fernando; Serio, Simone; Zani, Stefania; Climent, Montserrat; Salvarani, Nicolò; Carullo, Pierluigi; Civilini, Efrem; Condorelli, Gianluigi; Elia, Leonardo; Quintavalle, Manuela

doi:10.1161/circresaha.120.316489

Cited by 100 publications

(68 citation statements)

References 69 publications

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“…Circulating miR-16 was upregulated after vascular injury in the presence of hindlimb ischemia [ 31 ] and exerted a negative effect on vascular remodeling. However, the detection of miRNA required a long period of stimulation or inflammation duration corresponding to vascular injury from several days to several weeks [ 31 , 32 ]. In our study, the duration of CPB was respectively 87 minutes [46–158] and 94 [41–184] in both groups and was probably too short to detect circulating miR-16.…”

Section: Discussionmentioning

confidence: 99%

Cardiopulmonary bypass and internal thoracic artery: Can roller or centrifugal pumps change vascular reactivity of the graft? The IPITA study: A randomized controlled clinical trial

et al. 2020

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Background Cardiopulmonary bypass (CPB) induces a systemic inflammatory response (SIRS) and affects the organ vascular bed. Experimentally, the lack of pulsatility alters myogenic tone of resistance arteries and increases the parietal inflammatory response. The purpose of this study was to compare the vascular reactivity of the internal thoracic arteries (ITAs) due to the inflammatory response between patients undergoing coronary artery bypass grafting (CABG) under CPB with a roller pump or with a centrifugal pump. Methods Eighty elective male patients undergoing CABG were selected using one or two internal thoracic arteries under CPB with a roller pump (RP group) or centrifugal pump (CFP group). ITA samples were collected before starting CPB (Time 1) and before the last coronary anastomosis during aortic cross clamping (Time 2). The primary endpoint was the endotheliumdependent relaxation of ITAs investigated using wire-myography. The secondary endpoint was the parietal inflammatory response of arteries defined by the measurements of superoxide levels, leukocytes and lymphocytes rate and gene expression of inflammatory proteins using. Terminal complement complex activation (SC5b-9) and neutrophil activation (elastase) analysis were performed on arterial blood at the same times. Results Exposure time of ITAs to the pump flow was respectively 43.3 minutes in the RP group and 45.7 minutes in the CFP group. Acetylcholine-dependent relaxation was conserved in the

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Section: Discussionmentioning

confidence: 99%

Cardiopulmonary bypass and internal thoracic artery: Can roller or centrifugal pumps change vascular reactivity of the graft? The IPITA study: A randomized controlled clinical trial

et al. 2020

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“…It has been reported that overexpression of miR-128 can signi cantly decrease VSMCs migration, phenotypic transformation and proliferation by targeting Kruppel-like factor 4 (KLF4) [42]. KLF4 acts as a key repressor of VSMCs differentiation, modulating the expression of SM22α and PPARs [42,43]. MiR-128-5p has the similar function of miR-128 and TIMP-3, TIMP-4, SIRT2, PPAR , PPARδ and p21 are the negatively controlled by miR-128-5p.…”

Section: Discussionmentioning

confidence: 99%

The Compatibility of Alisma and Atractylodes Affects the Biological Behaviors of VSMCs Via Inhibiting miR-128-5p / p21 Gene

Wei

Shen

et al. 2020

Preprint

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Background：The compatibility of Alisma and Atractylodes (AA) has been estimated to exhibit anti-atherosclerotic effects, while the mechanism still remains unclear. This study was aimed to identify the role of AA on oxidized low density lipoprotein (ox-LDL)-induced vascular smooth muscle cells (VSMCs) behaviors, and to explore the effect of microRNAs (miRNAs). Methods：Scratch wound healing assay detected the migration of VSMCs, immunocytochemistry assay and western blot of SM22ɑ were used to evaluated the phenotypic transformation. Bromodeoxyuridine (Brdu) immunocytochemistry and flow cytometry were applied to detect the proliferation of VSMCs. The miRNA microarray profiling was performed using lianchuan biological small RNA sequencing analysis. VSMCs were transfected with the miR-128-5p mimic and inhibitor, the migration, phenotypic modulation and proliferation of VSMCs were investigated. The 3'UTR binding sequences site of miR-128-5p on p21 gene were predicted and assessed by luciferase assays.Results：AA and extracellular regulated protein kinases 1/2 (ERK1/2) blocker U0126 markedly inhibited the ability of migration, elevated smooth muscle 22alpha (SM22α) expression, repressed VSMCs proliferation, elevated the expression of miR-466f-3p and miR-425-3p, while suppressed miR-27a-5p and miR-128-5p expression in the ox-LDL-induced VSMCs. MiR-128-5p targets tissue inhibitor of metalloproteinase (TIMPs), silent information regulator 2 (SIRT2), peroxisome proliferator-activated receptors (PPARs) and p21 genes, which is linked to the behaviors of VSMCs. MiR-128-5p mimic promoted migration and proliferation of VSMCs, and suppressed the p21, p27 and SM22ɑ expression. The inhibitor increased p21, p27 and SM22ɑ expression, and repressed the migration, phenotypic transformation and proliferation of VSMCs. MiR-128-5p directly targeted the 3′UTR binding sequences of p21 gene, negatively regulated p21 expression and exerted a role in the proliferation of VSMCs.Conclusion：Our research showed that the migration, phenotypic transformation and proliferation of ox-LDL-induced VSMCs were repressed by AA through inhibiting miR-128-5p via targeting p21 gene, which may provide an effective option for the treatment of Atherosclerosis.

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“…The present study demonstrated that the inhibitory effect of dHa on the proliferation and migration of VSMcs is mediated by microrna-155 downregulation. Microrna-155 is a multifunctional non-coding rna that plays an important role in the pathogenesis of carotid restenosis (31). However, the Socs1 target gene of microrna-155 can regulate various signalling pathways, which may contribute to the function of a recent study demonstrated that low dHa levels were significantly associated with lipid-rich coronary and carotid plaques, yet the mechanism of DHA in the stabilization of carotid plaque and its beneficial effects in patients with carotid restenosis require additional investigation (32).…”

Section: Discussionmentioning

confidence: 99%

Docosahexaenoic acid inhibits vascular smooth muscle cell migration and proliferation by decreasing microRNA‑155 expression levels

Yin

et al. 2020

Mol Med Rep

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Vascular smooth muscle cell (VSMc) hyperplasia is a common cause of carotid restenosis. in the present study, the potential protective effects of docosahexaenoic acid (dHa) in carotid restenosis and the underlying mechanism of its effects were examined. VSMcs were treated with dHa, a polyunsaturated ω-3 fatty acid. cell migration and proliferation were assessed using wound healing and cell counting Kit-8 assays and by measuring Ki-67 protein levels. additionally, the expression levels of microrna-155 were determined by reverse transcription-quantitative Pcr (rT-qPcr). The involvement of microrna-155 in the regulation of migration and proliferation was evaluated by transfecting VSMcs with microrna mimics and inhibitors. Moreover, the reversal of migration and proliferation after transfection of VSMcs with the microrna mimics and subsequent treatment with dHa was investigated. A target gene of microRNA-155 was identified using RT-qPCR and luciferase assays. The migration and proliferation of VSMcs, as well as the expression of microrna-155 was inhibited by dHa stimulation. Microrna-155 regulated the migration and proliferation of VSMcs. Finally, proliferation and migration of VSMcs were reduced following dHa treatment, which was mediated by an increase in the expression levels of microrna-155. Suppressor of cytokine signalling 1 (Socs1) was the target gene of microrna-155. in conclusion, dHa inhibited VSMc migration and proliferation by reducing microrna-155 expression. This effect may be caused by the microrna-155 target gene Socs1.

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miR-128-3p Is a Novel Regulator of Vascular Smooth Muscle Cell Phenotypic Switch and Vascular Diseases

Cited by 100 publications

References 69 publications

Cardiopulmonary bypass and internal thoracic artery: Can roller or centrifugal pumps change vascular reactivity of the graft? The IPITA study: A randomized controlled clinical trial

Cardiopulmonary bypass and internal thoracic artery: Can roller or centrifugal pumps change vascular reactivity of the graft? The IPITA study: A randomized controlled clinical trial

The Compatibility of Alisma and Atractylodes Affects the Biological Behaviors of VSMCs Via Inhibiting miR-128-5p / p21 Gene

Docosahexaenoic acid inhibits vascular smooth muscle cell migration and proliferation by decreasing microRNA‑155 expression levels

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