MicroRNA-29b inhibits human vascular smooth muscle cell proliferation via targeting the TGF-β/Smad3 signaling pathway

Li, Lirong; Ren, Shaohua; Hao, Xudong; Zhen, Zigang; Ji, Lei; Ji, Hongming

doi:10.3892/etm.2021.9923

Cited by 8 publications

(6 citation statements)

References 33 publications

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“…As described in previous studies [7], VSMCs trigger stress and injury changes in response to blood pressure by accelerating cell migration and proliferation. Therefore, to investigate the effects of miR-152-3p on cell proliferation and migration, we transfected miR-152-3p mimic and inhibitor in HVSMCs and RT-qPCR confirmed that it was typically up-or down-regulated (p < 0.05, Fig.…”

Section: Mir-152-3p Inhibited the Proliferation And Migration Of Hvsmcssupporting

confidence: 55%

Cerebrospinal fluid exosomal miR-152-3p predicts the occurrence of subarachnoid haemorrhage and regulates vascular smooth muscle cell dysfunction

Li¹,

An²,

Dai³

et al. 2022

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Introduction: Ruptured intracranial aneurysm (RA) can lead to subarachnoid haemorrhage (SAH). This study was to explore the predictive value of cerebrospinal fluid (CSF) derived exosome miR-152-3p and its regulatory role in the human vascular smooth muscle cells (HVSMCs).Material and methods: Real-time quantitative polymerase reaction was carried out to detect CSF exosome miR-152-3p in 66 patients with unruptured intracranial aneurysms (UA), 69 patients with RA, and 68 patients with hydrocephalus. Clinical predictive value of SAH occurrence was assessed using receiver operating characteristic curve (ROC) and logistics regression analysis. Cell Counting Kit-8 and Transwell were employed to detect the proliferation and migration of HVSMCs. The binding relationship between miR-152-3p and PTEN was confirmed by the dual-luciferase reporter assay. Results: Compared with hydrocephalus, exosome miR-152-3p was lower in patients with intracranial aneurysms, and among them, RA was lower than in patients with UA (p < 0.001). ROC confirmed that exosome miR-152-3p not only distinguishes patients with UA from patients with hydrocephalus but also predicts SAH in patients with intracranial aneurysms. Logistic regression analysis showed that miR-152-3p (OR = 0.039, 95% CI = 0.015-0.106, p < 0.001) and aneurysm size (OR = 2.701, 95% CI = 1.045-6.890, p = 0.040) were independent predictors of progression for UA to RA. Increased miR-152-3p inhibited the proliferation and migration of HVSMCs. PTEN was the direct target gene of miR-152-3p, which was elevated in CSF-derived exosomes and negatively correlated with miR-152-3p levels. Conclusions: Our study confirmed that the CSF-derived exosome miR-152-3p was a feasible predictor of SAH and was involved in the dysfunction of HVSMCs.

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Section: Mir-152-3p Inhibited the Proliferation And Migration Of Hvsmcssupporting

confidence: 55%

Cerebrospinal fluid exosomal miR-152-3p predicts the occurrence of subarachnoid haemorrhage and regulates vascular smooth muscle cell dysfunction

Li¹,

An²,

Dai³

et al. 2022

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“…miR-29b-2 appears to be mostly associated with a contractile phenotype. It reduced proliferation and migration in human aortic SMCs [26], and inhibiting miR-29b-2 promoted dedifferentiation in human intracranial aneurysm SMCs [27]. It can target Kruppel-like factor 4 (KLF4; a key protein involved in SMC dedifferentiation) [25] and can also target TGFβ [26], a growth factor that can cause ND SV-SMCs to transiently adopt a T2DM SV-SMC phenotype [8].…”

Section: Discussionmentioning

confidence: 99%

Defining the miRnome of Saphenous Vein Smooth Muscle Cells from Patients with Type 2 Diabetes Mellitus

Hussain,

Asare-Amankwah,

Qureshi

et al. 2024

Diabetology

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Type 2 diabetes mellitus (T2DM) patients suffer premature development of cardiovascular disease and commonly require cardiac revascularization using the autologous saphenous vein (SV). Smooth muscle cells (SMCs) are the principal cell type within the vascular wall and are dysfunctional in T2DM SV-SMCs, yet the mechanisms underpinning this are incompletely understood. The purpose of this study was to interrogate differential microRNA (miRNA) expression in SV-SMCs to enhance our understanding of T2DM SV-SMC phenotypic change. miRNA expression in primary human SV-SMCs from T2DM and non-diabetic (ND) donors was determined using an array (n = 6 each of ND and T2DM SV-SMCs). Differentially expressed miRNAs were ranked, and functional annotation of the 30 most differentially expressed miRNAs using DAVID and KEGG analysis revealed pathways related to SMC phenotype, including proliferation, migration, cytokine production and cell signaling. After selecting miRNAs known to be involved in SMC phenotypic regulation, miR-17, miR-29b-2, miR-31, miR-130b and miR-491 were further validated using qRT-PCR (n = 5 each of ND and T2DM SV-SMC), with miR-29b-2 subsequently being removed from further investigation. Potential mRNA targets were identified using mirDIP. Predicted target analysis highlighted likely dysregulation in transcription, epigenetic regulation, cell survival, intracellular signaling and cytoskeletal regulation, all of which are known to be dysfunctional in T2DM SV-SMCs. In conclusion, this paper identified four miRNAs that are dysregulated in T2DM SV-SMCs and are implicated in functional changes in the behavior of these cells. This provides a step forward in our understanding of the molecular and epigenetic regulation of vascular dysfunction in T2DM.

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“…During this process, a variety of chemokines, chemokine structural analogues, and downstream signals related to the activation of paracrine cytokines contribute to the development or regeneration of VW-S/PCs [57]. Studies have revealed successively that many biochemical cues, such as ERK and PI3K/ AKT signaling, Rac1/Cdc42 signaling pathway, and Wnt and Notch signaling pathway, are involved in the regulation of stem cell migration and differentiation under physiological and pathological condition [57][58][59][60]. For example, Dickkopf-3 (DKK3), a secreted glycoprotein, can activate ERK1/2, PI3K/AKT, Rac1, and RhoA signaling pathways by binding to chemokine (C-X-C motif) ligand 7 (CXCR7), to regulate the migration of Sca-1 + vascular stem cells in the vascular adventitia.…”

Section: Biochemical Signals In the Microenvironment Affecting Vw-s/pcsmentioning

confidence: 99%

The Microenvironment That Regulates Vascular Wall Stem/Progenitor Cells in Vascular Injury and Repair

Yang

et al. 2022

BioMed Research International

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Vascular repair upon injury is a frequently encountered pathology in cardiovascular diseases, which is crucial for the maintenance of arterial homeostasis and function. Stem/progenitor cells located on vascular walls have multidirectional differentiation potential and regenerative ability. It has been demonstrated that stem/progenitor cells play an essential role in the basic medical research and disease treatment. The dynamic microenvironment around the vascular wall stem/progenitor cells (VW-S/PCs) possesses many stem cell niche-like characteristics to support and regulate cells’ activities, maintaining the properties of stem cells. Under physiological conditions, vascular homeostasis is a cautiously balanced and efficient interaction between stem cells and the microenvironment. These interactions contribute to the vascular repair and remodeling upon vessel injury. However, the signaling mechanisms involved in the regulation of microenvironment on stem cells remain to be further elucidated. Understanding the functional characteristics and potential mechanisms of VW-S/PCs is of great significance for both basic and translational research. This review underscores the microenvironment-derived signals that regulate VW-S/PCs and aims at providing new targets for the treatment of related cardiovascular diseases.

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MicroRNA-29b inhibits human vascular smooth muscle cell proliferation via targeting the TGF-β/Smad3 signaling pathway

Cited by 8 publications

References 33 publications

Cerebrospinal fluid exosomal miR-152-3p predicts the occurrence of subarachnoid haemorrhage and regulates vascular smooth muscle cell dysfunction

Cerebrospinal fluid exosomal miR-152-3p predicts the occurrence of subarachnoid haemorrhage and regulates vascular smooth muscle cell dysfunction

Defining the miRnome of Saphenous Vein Smooth Muscle Cells from Patients with Type 2 Diabetes Mellitus

The Microenvironment That Regulates Vascular Wall Stem/Progenitor Cells in Vascular Injury and Repair

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