scholarly journals Knockdown of long non-coding RNA OIP5-AS1 suppresses cell proliferation and migration in ox-LDL-induced human vascular smooth muscle cells (hVMSCs) through targeting miR-152-3p/PAPPA axis

RSC Advances ◽  
2019 ◽  
Vol 9 (56) ◽  
pp. 32499-32509 ◽  
Author(s):  
Xiangya Yang ◽  
Zhongrui Li ◽  
Lei Zhang ◽  
Xiaoshan Wu ◽  
Qixin Kang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cell Proliferation And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Knockdown of OIP5-AS1 suppressed ox-LDL-treated hVMSCs proliferation and migration; overexpression of miR-152 played the similar role of OIP5-AS1 knockdown; OIP5-AS1 functioned as ceRNA to regulate PAPPA expression through sponging miR-152.

scholarly journals Retraction: Knockdown of long non-coding RNA OIP5-AS1 suppresses cell proliferation and migration in ox-LDL-induced human vascular smooth muscle cells (hVMSCs) through targeting miR-152-3p/PAPPA axis

RSC Advances ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 5231-5231
Author(s):  
Laura Fisher
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cell Proliferation And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Retraction of ‘Knockdown of long non-coding RNA OIP5-AS1 suppresses cell proliferation and migration in ox-LDL-induced human vascular smooth muscle cells (hVMSCs) through targeting miR-152-3p/PAPPA axis’ by Xiangya Yang et al., RSC Adv., 2019, 9, 32499–32509, DOI: 10.1039/C9RA06614D.

scholarly journals SIRT7 Regulates the Vascular Smooth Muscle Cells Proliferation and Migration via Wnt/β-Catenin Signaling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Jianghua Zheng ◽  
Kai Chen ◽  
Haifei Wang ◽  
Zhilong Chen ◽  
Yong Xi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Counting ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

A huge amount of evidence indicates that sirtuin 7 (SIRT7), a key mediator of many cellular activities, plays a crucial role in the pathogenesis of various diseases. However, little is known about the role of SIRT7 in atherosclerosis. This study investigated the potential role of SIRT7 in regulating the proliferation and migration of human vascular smooth muscle cells (HAVSMCs) and its possible molecular mechanism. In this study, human vascular smooth muscle cells (HAVSMCs) were induced by oxidized low-density lipoprotein (ox-LDL) to establish atherosclerosis (AS) cell model. Immunofluorescence staining and Western blot were used to detect the level of α-SMA expression, which was a marker protein in AS. In addition, RT-qPCR and Western blot assay were applied for exploring the mRNA and protein expression levels of SIRT7, Wnt, β-catenin, and cyclin D1 after knockdown or overexpression of SIRT7. And, furthermore, Cell Counting Kit-8 assay, flow cytometry, and wound-healing assay were used to assess HAVSMCs proliferation, cell cycle, and migration. Dickkopf-1 (DKK-1), a secretory glycoprotein that can block Wnt/β-catenin pathway, was used in SIRT7 overexpression HAVSMCs; subsequently cells proliferation and migration were assessed by Cell Counting Kit-8 assay, flow cytometry analysis, and wound-healing assay. We found that knockdown of SIRT7 significantly promoted cell proliferation and migration, decreased the percentages of cells in the G1 and G2 phases, and increased those in the S phase and downregulated the protein expression levels of Wnt, β-catenin, and cyclin D1, while overexpression of SIRT7 had reverse results. After treatment with Wnt/beta-catenin pathway inhibitor DKK-1 in SIRT7 overexpression HAVSMCs, cell proliferation and migration were increased, respectively. In conclusion, SIRT7 inhibited HAVSMCs proliferation and migration via enhancing Wnt/β-catenin activation, which provided a novel therapeutic strategy for antiatherosclerosis.

scholarly journals Long Non-Coding RNA MEG8 Suppresses Hypoxia-Induced Excessive Proliferation, Migration and Inflammation of Vascular Smooth Muscle Cells by Regulation of the miR-195-5p/RECK Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Dexing Xu ◽  
Ruozhu Dai ◽  
Hao Chi ◽  
Wen Ge ◽  
Jingfeng Rong
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Adhesion Molecule ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Excessive Proliferation ◽  
Proliferation And Migration

It has been recognized that rebalancing the abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) helps relieve vascular injury. Presently, we aim to investigate whether long non-coding RNA (lncRNA) maternally expressed 8 (MEG8) plays a role in affecting the excessive proliferation and migration of VSMCs following hypoxia stimulation. A percutaneous transluminal angioplasty balloon dilatation catheter was adopted to establish vascular intimal injury, the levels of MEG8 and miR-195-5p in the carotid artery were tested by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Hypoxia was used to stimulate VSMCs, then the cell counting kit-8 (CCK-8) assay, Transnwell assay, and wound healing assay were conducted to evaluate the proliferation, and migration of VSMCs. The protein levels of RECK (reversion inducing cysteine rich protein with kazal motifs), MMP (matrix metalloproteinase) 3/9/13, COX2 (cytochrome c oxidase subunit II), macrophage inflammatory protein (MIP)-1beta, VCAM-1 (vascular cell adhesion molecule 1), ICAM-1 (intercellular adhesion molecule 1), and HIF-1α (hypoxia inducible factor 1 subunit alpha) were determined by western blot or cellular immunofluorescence. As the data showed, MEG8 was down-regulated in the carotid artery after balloon injury in rats and hypoxia-treated VSMCs, and miR-195-5p was overexpressed. Forced MEG8 overexpression or inhibiting miR-195-5p attenuated hypoxia-promoted cell proliferation and migration of VSMCs. In addition, miR-195-5p up-regulation reversed MEG8-mediated effects. Hypoxia hindered the RECK expression while boosted MMP3/9/13 levels, and the effect was markedly reversed with MEG8 up-regulation or miR-195-5p down-regulation. Mechanistically, MEG8 functioned as a competitive endogenous (ceRNA) by sponging miR-195-5p which targeted RECK. Moreover, the HIF-1α inhibitor PX478 prevented hypoxia-induced proliferation, and migration of VSMCs, upregulated MEG8, and restrained miR-195-5p expression. Overall, lncRNA MEG8 participated in hypoxia-induced excessive proliferation, inflammation and migration of VSMCs through the miR-195-5p/RECK axis.

Abstract 16436: Targeting Store Operated Calcium Entry in Vascular Smooth Muscle Cells by a Novel Small-molecule Inhibitor

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Heba Shawer ◽  
Karen Hemmings ◽  
Karen Porter ◽  
Richard Foster ◽  
David J Beech ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle Cells ◽  
Small Molecule ◽  
Cell Proliferation And Migration ◽  
Molecule Inhibitor ◽  
Store Operated Calcium Entry ◽  
And Migration ◽  
Proliferation And Migration

Vascular smooth muscle cells (VSMC) are physiologically quiescent cells optimised for vascular contractility and the modulation of vascular tone. Platelet-derived growth factor (PDGF) signalling is a critical driver of pathological remodelling of native VSMC to a proliferative synthetic state, which is a process associated with vascular pathologies. Here, we studied the role of store operated calcium entry (SOCE) through Orai1 channels in VSMC plasticity utilizing novel small molecule inhibitor of Orai1 channels. We developed small-molecule Orai1 inhibitor, 4-(2,5-dimethoxyphenyl)-N-[(pyridin-4-yl)methyl]aniline, called JPIII, evaluated its effects on SOCE, and its functional impact in human primary VSMC (hVSMC) from saphenous vein and rat thoracic aorta VSMC cell line. Our Orai1 inhibitor potently suppressed SOCE in hVSMC (IC 50 of 297 nM, n=3) and rat VSMC (IC 50 of 819.5 nM, n=3), leading to significant impairment of PDGF-induced cell migration in hVSMC by 31% (P=0.0071, n=6) and rat VSMC by 24% (P=0.04, n=3). Orai1 inhibition also reduced PDGF-induced proliferation of hVSMC by 20% (P=0.02, n=5) and of rat VSMC by 26% (P=0.003, n=4) at concentration of 30 μM JPIII relative to controls. RNA-Seq analysis of PDGF-stimulated primary human aortic VSMC (n=4/group) was performed to investigate the effects of Orai1 inhibition on the transcriptional response of cells and showed significant downregulation of genes involved in inflammation (C-X-C motif chemokine ligand (CXCL) 1, CXCL3, CXCL5, CXCL6), downregulation of matrix degrading enzymes (metalloproteinase (MMP) 12 and MMP16), and upregulation of cholesterol biosynthesis pathways by Orai1 inhibition. Consistent with the observed functional phenotype, our results revealed an inhibitory effect on transcriptional networks involved in cell proliferation and migration. The effects of Orai1 inhibition on the transcription of genes involved in inflammation, MMPs expression, cholesterol metabolism, cell proliferation, and migration powerfully associate Orai1 signalling with VSMC remodelling. Our results provide insight into the role of Orai1 in VSMC remodelling and the possible therapeutic potential of a small molecule inhibition approach in targeting pathologic remodelling.

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