MiR-29b mimics promotes cell apoptosis of smooth muscle cells via targeting on MMP-2

Shen, Lingguang; Song, Yanhui; Fu, Yuqin; Li, Peipei

doi:10.1007/s10616-017-0150-z

Cited by 13 publications

(9 citation statements)

References 34 publications

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“…In chicken, the gga-miR-29b cluster contains gga-miR-29b-1-5p, gga-miR-29b-2-5p, and gga-miR-1701. MiR-29s are efficient regulators in the process of cell proliferation [ 30 ], differentiation [ 31 ], apoptosis [ 32 , 33 , 34 ] as well as DNA methylation [ 35 , 36 ] in different cell types. In skeletal muscle, miR-29s could participate in regulating skeletal myogenesis through different pathways.…”

Section: Introductionmentioning

confidence: 99%

A Novel Circular RNA Generated by FGFR2 Gene Promotes Myoblast Proliferation and Differentiation by Sponging miR-133a-5p and miR-29b-1-5p

Chen

Ouyang

Wang

et al. 2018

Cells

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It is well known that fibroblast growth factor receptor 2 (FGFR2) interacts with its ligand of fibroblast growth factor (FGF) therefore exerting biological functions on cell proliferation and differentiation. In this study, we first reported that the FGFR2 gene could generate a circular RNA of circFGFR2, which regulates skeletal muscle development by sponging miRNA. In our previous study of circular RNA sequencing, we found that circFGFR2, generated by exon 3–6 of FGFR2 gene, differentially expressed during chicken embryo skeletal muscle development. The purpose of this study was to reveal the real mechanism of how circFGFR2 affects skeletal muscle development in chicken. In this study, cell proliferation was analyzed by both flow cytometry analysis of the cell cycle and 5-ethynyl-2′-deoxyuridine (EdU) assays. Cell differentiation was determined by analysis of the expression of the differentiation marker gene and Myosin heavy chain (MyHC) immunofluorescence. The results of flow cytometry analysis of the cell cycle and EdU assays showed that, overexpression of circFGFR2 accelerated the proliferation of myoblast and QM-7 cells, whereas knockdown of circFGFR2 with siRNA reduced the proliferation of both cells. Meanwhile, overexpression of circFGFR2 accelerated the expression of myogenic differentiation 1 (MYOD), myogenin (MYOG) and the formation of myotubes, and knockdown of circFGFR2 showed contrary effects in myoblasts. Results of luciferase reporter assay and biotin-coupled miRNA pull down assay further showed that circFGFR2 could directly target two binding sites of miR-133a-5p and one binding site of miR-29b-1-5p, and further inhibited the expression and activity of these two miRNAs. In addition, we demonstrated that both miR-133a-5p and miR-29b-1-5p inhibited myoblast proliferation and differentiation, while circFGFR2 could eliminate the inhibition effects of the two miRNAs as indicated by rescue experiments. Altogether, our data revealed that a novel circular RNA of circFGFR2 could promote skeletal muscle proliferation and differentiation by sponging miR-133a-5p and miR-29b-1-5p.

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Section: Introductionmentioning

confidence: 99%

A Novel Circular RNA Generated by FGFR2 Gene Promotes Myoblast Proliferation and Differentiation by Sponging miR-133a-5p and miR-29b-1-5p

Chen

Ouyang

Wang

et al. 2018

Cells

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“…miR-145, one of the most abundant VSMC miRNAs, mitigates a phenotypic switch from the contractile state into the proliferative one by inducing Myocd expression (24). miR-29b mimics reduces cell viability and promotes SMC apoptosis by inhibiting matrix metalloproteinase 2 (MMP2) expression, one of MMPs to enhance VSMC switch from the contractile phenotype into the synthetic phenotype (25,26). In this study, we found TL1A decreased miR-214-5p expression, but increased expression of miR-145 and miR-29b ( Fig.…”

Section: Tl1a Enhances Plaque Stability By Regulating Vsmc Phenotypicmentioning

confidence: 99%

TL1A inhibits atherosclerosis in apoE-deficient mice by regulating the phenotype of vascular smooth muscle cells

Zhao

Xue

et al. 2020

Journal of Biological Chemistry

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TNF ligand-related molecule 1A (TL1A) is a vascular endothelial growth inhibitor to reduce neovascularization. Lack of ApoE expression results in hypercholesterolemia and atherosclerosis. In this study, we determined the precise effects of TL1A on the development of atherosclerosis and the underlying mechanisms in ApoE deficient mice. After 12 weeks of pro-atherogenic high-fat diet feeding and TL1A treatment, mouse aorta, serum and liver samples were collected and used to assess atherosclerotic lesions, fatty liver and expression of related molecules. We found TL1A treatment significantly reduced lesions and enhanced plaque stability. Mechanistically, TL1A inhibited formation of foam cells derived from vascular smooth muscle cells (VSMCs), but not macrophages by activating expression of ATP-binding cassette transporter A1 (ABCA1), ABCG1 and cholesterol efflux in the liver X receptor-dependent manner. TL1A reduced the transformation of VSMCs from contractile phenotype into synthetic phenotypes by activating expression of contractile marker α smooth muscle actin and inhibiting expression of synthetic marker osteopontin, or osteoblast-like phenotype by reducing calcification. In addition, TL1A ameliorated high-fat diet-induced lipid metabolic disorders in the liver. Taken together, our work shows that TL1A can inhibit the development of atherosclerosis by regulating VSMC/foam cell formation and switch of VSMC phenotypes, and suggests the further investigation on its potential for atherosclerosis treatment.

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“…MMPs contribute to plaque stability by catalysing reactions that either disintegrate or stabilise ECM components. In addition to its effects in regulating ECM content, miR-29b also inhibits MMP2 expression [104]. The atherogenic properties of VSMCs are decreased by miR-133b inhibition, which targets MMP9 [105], a key regulator of collagen degradation that is significantly upregulated in atherosclerotic plaques [106].…”

Section: Fibrous Cap Thinningmentioning

confidence: 99%

MicroRNAs as Therapeutic Targets and Clinical Biomarkers in Atherosclerosis

Solly

Dimasi

Bursill

et al. 2019

JCM

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Atherosclerotic cardiovascular disease remains the leading cause of morbidity and mortality worldwide. Atherosclerosis develops over several decades and is mediated by a complex interplay of cellular mechanisms that drive a chronic inflammatory milieu and cell-to-cell interactions between endothelial cells, smooth muscle cells and macrophages that promote plaque development and progression. While there has been significant therapeutic advancement, there remains a gap where novel therapeutic approaches can complement current therapies to provide a holistic approach for treating atherosclerosis to orchestrate the regulation of complex signalling networks across multiple cell types and different stages of disease progression. MicroRNAs (miRNAs) are emerging as important post-transcriptional regulators of a suite of molecular signalling pathways and pathophysiological cellular effects. Furthermore, circulating miRNAs have emerged as a new class of disease biomarkers to better inform clinical diagnosis and provide new avenues for personalised therapies. This review focusses on recent insights into the potential role of miRNAs both as therapeutic targets in the regulation of the most influential processes that govern atherosclerosis and as clinical biomarkers that may be reflective of disease severity, highlighting the potential theranostic (therapeutic and diagnostic) properties of miRNAs in the management of cardiovascular disease.

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MiR-29b mimics promotes cell apoptosis of smooth muscle cells via targeting on MMP-2

Cited by 13 publications

References 34 publications

A Novel Circular RNA Generated by FGFR2 Gene Promotes Myoblast Proliferation and Differentiation by Sponging miR-133a-5p and miR-29b-1-5p

A Novel Circular RNA Generated by FGFR2 Gene Promotes Myoblast Proliferation and Differentiation by Sponging miR-133a-5p and miR-29b-1-5p

TL1A inhibits atherosclerosis in apoE-deficient mice by regulating the phenotype of vascular smooth muscle cells

MicroRNAs as Therapeutic Targets and Clinical Biomarkers in Atherosclerosis

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