miRNA-146a induces vascular smooth muscle cell apoptosis in a rat model of coronary heart disease via NF-κB pathway

Wu, Zhichun; Liu, Y F; Wang, S; Li, B

doi:10.4238/2015.december.28.19

Cited by 25 publications

(27 citation statements)

References 21 publications

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“…The results of the present study indicate that the therapeutic effects of ESCs improve the atherosclerosis indices in a rat model of CAD compared with control rats. Wu et al (24) reported that miRNA-146a induced vascular smooth muscle cell apoptosis via the NF-κB signaling pathway. In the present study, ESCs therapy decreased miRNA-146a expression and increased VEGF expression in the myocardium of rats with CAD.…”

Section: Discussionmentioning

confidence: 99%

Endothelial stem cells attenuate cardiac apoptosis via downregulating cardiac microRNA‑146a in a rat model of coronary heart disease

et al. 2018

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Coronary artery disease (CAD) is one of the main causes of hospitalization worldwide and has high morbidity. It has previously been demonstrated that stem cells serve an important role in improving myocardial function. MicroRNA (miRNA)-146a downregulation has been reported to inhibit vascular smooth muscle cell apoptosis in a rat model of coronary heart disease. The aim of the present study was to investigate the mechanisms underlying the effects of endothelial stem cell (ESC)-derived paracrine factors and cardiac miRNAs in CAD. Acute myocardial infarction was induced in 20 rats. Autologous ESCs (n=10; experimental group) or PBS (n=10; control group) were injected in the border zone. Reverse transcription-quantitative polymerase chain reaction, ELISA and immunohistochemistry assays were performed to analyze the therapeutic effects of ESCs in rats with coronary heart disease rats. Serum interleukin (IL)-1, IL-17 and tumor necrosis factor-α were reduced in the experimental group compared with control rats, as was the number of circulating proatherogenic cells. The results demonstrated that ESC transplantation markedly downregulated miRNA-146a expression and decreased apoptosis in the myocardium compared with the control group. Rats in the experimental group also had higher levels of vascular endothelial growth factor compared with the control group. In addition, it was demonstrated that miRNA-146 knockdown reduced cardiac apoptosis and increased VEGF expression. Furthermore, the infarct area in the border zone or rats with CAD was reduced in the experimental group compared with the control group. In conclusion, these results suggest that ESC transplantation may improve cardiac function via downregulating miR-146a, which may be have potential as a treatment for CAD.

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Section: Discussionmentioning

confidence: 99%

Endothelial stem cells attenuate cardiac apoptosis via downregulating cardiac microRNA‑146a in a rat model of coronary heart disease

et al. 2018

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“…Moreover, miR-92a overexpression inhibits H 2 O 2 -induced VSMCs apoptosis and senescence by suppressing both mitogen-activated protein kinase 4 (MKK4) and JNK1 pathways [81]. Another miRNA, miRNA-146a was found to induce VSMC apoptosis via activation of the NF- κ B signaling pathway [82]. …”

Section: Mirnas and Vascular Agingmentioning

confidence: 99%

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

Lin

Zhan

Wang

et al. 2016

BioMed Research International

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Vascular aging, a specific type of organic aging, is related to age-dependent changes in the vasculature, including atherosclerotic plaques, arterial stiffness, fibrosis, and increased intimal thickening. Vascular aging could influence the threshold, process, and severity of various cardiovascular diseases, thus making it one of the most important risk factors in the high mortality of cardiovascular diseases. As endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cell biological basis of these pathology changes of the vasculature, the structure and function of ECs and VSMCs play a key role in vascular aging. MicroRNAs (miRNAs), small noncoding RNAs, have been shown to regulate the expression of multiple messenger RNAs (mRNAs) posttranscriptionally, contributing to many crucial aspects of cell biology. Recently, miRNAs with functions associated with aging or aging-related diseases have been studied. In this review, we will summarize the reported role of miRNAs in the process of vascular aging with special emphasis on EC and VSMC functions. In addition, the potential application of miRNAs to clinical practice for the diagnosis and treatment of cardiovascular diseases will also be discussed.

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“…It is necessary to identify disease-specific miRNAs and their targets to understand their roles in disease (29)(30)(31). It has been reported that various miRNAs participate in mediating the functions of VSMCs, including miR-21, miR-214 and miR-146a (32)(33)(34). In the present study, the expression level of miR-24-3p in the blood samples of 30 patients with CHD was explored using RT-qPCR and it was found that the miRNA-24-3p level was higher in the blood samples of patients with CHD compared with the normal controls.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑24‑3p inhibition prevents cell growth of vascular smooth muscle cells by targeting Bcl‑2‑like protein 11

et al. 2020

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Numerous reports have shown that dysfunction of vascular smooth muscle cells (VSMCs) serves a critical function in the development of cardiovascular disease, including coronary heart disease (CHD). microRNAs (miRNAs/miRs) have been reported to play important roles in regulating the function of VSMCs. The present study aimed to determine the role of miR-24-3p in VSMCs and to uncover the underlying mechanism. The expression of miR-24-3p in the peripheral blood samples of CHD patients was measured by reverse transcription-quantitative (RT-q) PCR. It was found that the level of miR-24-3p in the peripheral blood of patients with CHD was significantly upregulated compared with that in healthy controls. A dual luciferase reporter assay was performed to determine whether Bcl-2-like protein 11 (Bcl-2L11) was a target gene of miR-24-3p, and it was identified that Bcl-2L11 was a direct target of miR-24-3p. The mRNA level and protein expression of Bcl-2L11 in the peripheral blood of patients with CHD were measured by RT-qPCR and western blotting, respectively. The findings suggested that Bcl-2L11 was downregulated in the peripheral blood of patients with CHD. In addition, it was found that downregulation of miR-24-3p suppressed VSMC proliferation and promoted VSMC apoptosis, while the effects of the miR-24-3p inhibitor on cell viability and apoptosis were reversed by Bcl-2L11-small interfering (si)RNA. Additionally, downregulation of miR-24-3p increased the levels of Bcl-2L11, caspase-3 and Bax, and decreased Bcl-2 expression in VSMCs; these changes were abolished by Bcl-2L11-siRNA. In conclusion, the aforementioned results indicated that miR-24-3p was an important regulator in VSMC proliferation and apoptosis by targeting Bcl-2L11, which suggested that miR-24-3p might be a potential therapeutic target for the treatment of CHD.

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miRNA-146a induces vascular smooth muscle cell apoptosis in a rat model of coronary heart disease via NF-κB pathway

Cited by 25 publications

References 21 publications

Endothelial stem cells attenuate cardiac apoptosis via downregulating cardiac microRNA‑146a in a rat model of coronary heart disease

Endothelial stem cells attenuate cardiac apoptosis via downregulating cardiac microRNA‑146a in a rat model of coronary heart disease

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

MicroRNA‑24‑3p inhibition prevents cell growth of vascular smooth muscle cells by targeting Bcl‑2‑like protein 11

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