miR-16-5p Is a Novel Mediator of Venous Smooth Muscle Phenotypic Switching

Zhang, Dengshen; Shi, Jun; Liang, Guiyou; Liu, Daxing; Zhang, Jian; Pan, Sisi; Lu, Yuan‐Fu; Wu, Qin; Gong, Changyang; Guo, Yingqiang

doi:10.1007/s12265-022-10208-1

Cited by 4 publications

(4 citation statements)

References 57 publications

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“…Mechanistically, miR-16-5p could disrupt the expression of zyxin, a mechanotransducer of biological signals, via binding to the 3’UTR of the zyxin- mRNA, which inhibited the proliferation and migration of cultured VSMCs by preventing the switch from a contractile to a synthetic phenotype. Our study implies that miR-16-5p is a potential therapeutic target for combating intimal hyperplasia in vein grafts ( 121 ). miRNAs can be used as targets for preventing VSMCs from switching phenotype and preventing intimal hyperplasia after vein grafting.…”

Section: Introductionmentioning

confidence: 72%

“…Many cardiovascular diseases are relevant to the abnormal expression and function of miRNAs (114). As shown in Figure 2, miRNAs exhibit regulatory effects on the function and phenotype of venous SMCs (115)(116)(117)(118)(119)(120)(121). Furthermore, many studies have shown that miRNA regulation of phenotypic transformation of VSMCs is vital for intimal hyperplasia in vein grafts.…”

Section: Role Of Mirnas In the Phenotypic Switch Of Vascular Smooth M...mentioning

confidence: 99%

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The Etiology and Molecular Mechanism Underlying Smooth Muscle Phenotype Switching in Intimal Hyperplasia of Vein Graft and the Regulatory Role of microRNAs

Zhang

Cao

Liu

et al. 2022

Front. Cardiovasc. Med.

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Mounting evidence suggests that the phenotypic transformation of venous smooth muscle cells (SMCs) from differentiated (contractile) to dedifferentiated (proliferative and migratory) phenotypes causes excessive proliferation and further migration to the intima leading to intimal hyperplasia, which represents one of the key pathophysiological mechanisms of vein graft restenosis. In recent years, numerous miRNAs have been identified as specific phenotypic regulators of vascular SMCs (VSMCs), which play a vital role in intimal hyperplasia in vein grafts. The review sought to provide a comprehensive overview of the etiology of intimal hyperplasia, factors affecting the phenotypic transformation of VSMCs in vein graft, and molecular mechanisms of miRNAs involved in SMCs phenotypic modulation in intimal hyperplasia of vein graft reported in recent years.

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Section: Introductionmentioning

confidence: 72%

Section: Role Of Mirnas In the Phenotypic Switch Of Vascular Smooth M...mentioning

confidence: 99%

The Etiology and Molecular Mechanism Underlying Smooth Muscle Phenotype Switching in Intimal Hyperplasia of Vein Graft and the Regulatory Role of microRNAs

Zhang

Cao

Liu

et al. 2022

Front. Cardiovasc. Med.

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“…The main cellular components of the vascular wall are vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs) 6,7 . The pathological process of IH starts with the injury of VECs.…”

Section: Introductionmentioning

confidence: 99%

“…5 The main cellular components of the vascular wall are vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs). 6,7 The pathological process of IH starts with the injury of VECs. VECs apoptosis is inevitable due to surgical procedures, ischemia-reperfusion, luminal pressure and changes in blood flow…”

mentioning

confidence: 99%

Improved therapeutic effects on vascular intimal hyperplasia by mesenchymal stem cells expressing MIR155HG that function as a ceRNA for microRNA‐205

Bai,

Qi,

Cai

et al. 2024

J Cellular Molecular Medi

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Coronary artery bypass grafting (CABG) is an effective treatment for coronary heart disease, with vascular transplantation as the key procedure. Intimal hyperplasia (IH) gradually leads to vascular stenosis, seriously affecting the curative effect of CABG. Mesenchymal stem cells (MSCs) were used to alleviate IH, but the effect was not satisfactory. This work aimed to investigate whether lncRNA MIR155HG could improve the efficacy of MSCs in the treatment of IH and to elucidate the role of the competing endogenous RNA (ceRNA). The effect of MIR155HG on MSCs function was investigated, while the proteins involved were assessed. IH was detected by HE and Van Gieson staining. miRNAs as the target of lncRNA were selected by bioinformatics analysis. qRT‐PCR and dual‐luciferase reporter assay were performed to verify the binding sites of lncRNA‐miRNA. The apoptosis, Elisa and tube formation assay revealed the effect of ceRNA on the endothelial protection of MIR155HG‐MSCs. We observed that MIR155HG improved the effect of MSCs on IH by promoting viability and migration. MIR155HG worked as a sponge for miR‐205. MIR155HG/miR‐205 significantly improved the function of MSCs, avoiding apoptosis and inducing angiogenesis. The improved therapeutic effects of MSCs on IH might be due to the ceRNA role of MIR155HG/miR‐205.

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Peripheral Blood miRNA Expression in Patients with Essential Hypertension in the Han Chinese Population in Hefei, China

Cheng,

Yang,

et al. 2024

Biochem Genet

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Primary hypertension is a significant risk factor for cardiovascular diseases. However, the pathogenesis of primary hypertension involves multiple biological processes, including the nervous system, circulatory system, endocrine system, and more. Despite extensive research, there is no clear understanding of the regulatory mechanism underlying its pathogenesis. In recent years, miRNAs have gained attention as a regulatory factor capable of modulating the expression of related molecules through gene silencing. Therefore, exploring differentially expressed miRNAs in patients with essential hypertension (EH) may offer a novel approach for future diagnosis and treatment of EH. This study included a total of twenty Han Chinese population samples from Hefei, China. The samples consisted of 10 healthy individuals and 10 patients with EH. Statistical analysis was conducted to analyze the general information of the two-sample groups. High-throughput sequencing and base identification were performed to obtain the original sequencing sequences. These sequences were then annotated using various databases including Rfam, cDNA sequences, species repetitive sequences library, and miRBase database. The number of miRNA species contained in the samples was measured. Next, TPM values were calculated to determine the expression level of each miRNA. The bioinformatics of the differentiated miRNAs were analyzed using the OECloud tool, and RPM values were calculated. Furthermore, the reliability of the expression was analyzed by calculating the area under the Roc curve using the OECloud tools. Statistical analysis revealed no significant differences between the two samples in terms of age distribution, gender composition, smoking history, and alcohol consumption history (P > 0.05). However, there was a notable presence of family genetic history and high BMI in the EH population (P < 0.05). The sequencing results identified a total of 245 miRNAs, out of which 16 miRNAs exhibited differential expression. Among the highly expressed miRNAs were let-7d-5p, miR-101-3p, miR-122-5p, miR-122b-3p, miR-192-5p, and miR-6722-3p. On the other hand, the lowly expressed miRNAs included miR-103a-3p, miR-16-5p, miR-181a-2-3p, miR-200a-3p, miR-200b-3p, miR-200c-3p, miR-221-3p, miR-30d-5p, miR-342-5p, and miR-543. This study initially identified 16 miRNAs that are aberrantly expressed and function in various processes associated with the onset and progression of essential hypertension. These miRNAs have the potential to be targeted for future diagnosis and treatment of EH. However, further samples are required to provide additional support for this study.

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miR-16-5p Is a Novel Mediator of Venous Smooth Muscle Phenotypic Switching

Cited by 4 publications

References 57 publications

The Etiology and Molecular Mechanism Underlying Smooth Muscle Phenotype Switching in Intimal Hyperplasia of Vein Graft and the Regulatory Role of microRNAs

The Etiology and Molecular Mechanism Underlying Smooth Muscle Phenotype Switching in Intimal Hyperplasia of Vein Graft and the Regulatory Role of microRNAs

Improved therapeutic effects on vascular intimal hyperplasia by mesenchymal stem cells expressing MIR155HG that function as a ceRNA for microRNA‐205

Peripheral Blood miRNA Expression in Patients with Essential Hypertension in the Han Chinese Population in Hefei, China

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