Silencing miR-16 Expression Promotes Angiotensin II Stimulated Vascular Smooth Muscle Cell Growth

Gu, Qun; Zhao, Guannan; Wang, Yinan; Xu, Baojun; Yue, Junming

doi:10.4172/2168-9296.1000181

Cited by 7 publications

(6 citation statements)

References 34 publications

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“…Knockdown of endogenous miRNA-15b/16 in VSMCs attenuated VSMC-specific gene expression and promoted VSMC proliferation and migration [27]. A different mechanism of proliferation suppression was demonstrated for miRNA-16, which was observed to be highly expressed in VSMCs and to be involved in the Ang-II-mediated VSMC signaling pathways [28]. Lentiviral vector-mediated miRNA-16 knockdown promoted Ang-II-induced cell proliferation and migration, which was associated with the pathways involving ERK1/2 and p38MAPK [28].…”

Section: Mirnas Which Inhibit Vsmc Proliferationmentioning

confidence: 99%

“…A different mechanism of proliferation suppression was demonstrated for miRNA-16, which was observed to be highly expressed in VSMCs and to be involved in the Ang-II-mediated VSMC signaling pathways [28]. Lentiviral vector-mediated miRNA-16 knockdown promoted Ang-II-induced cell proliferation and migration, which was associated with the pathways involving ERK1/2 and p38MAPK [28]. It was reported that the expression of miRNA-126 inhibited VSMC proliferation by targeting the low-density lipoprotein receptor-related protein 6 (LRP6) that is involved in a canonical Wnt pathway.…”

Section: Mirnas Which Inhibit Vsmc Proliferationmentioning

confidence: 99%

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The microRNAs Regulating Vascular Smooth Muscle Cell Proliferation: A Minireview

Wang

Atanasov

2019

IJMS

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Vascular smooth muscle cell (VSMC) proliferation plays a critical role in atherosclerosis. At the beginning of the pathologic process of atherosclerosis, irregular VSMC proliferation promotes plaque formation, but in advanced plaques VSMCs are beneficial, promoting the stability and preventing rupture of the fibrous cap. Recent studies have demonstrated that microRNAs (miRNAs) expressed in the vascular system are involved in the control of VSMC proliferation. This review summarizes recent findings on the miRNAs in the regulation of VSMC proliferation, including miRNAs that exhibit the inhibition or promotion of VSMC proliferation, and their targets mediating the regulation of VSMC proliferation. Up to now, most of the studies were performed only in cultured VSMC. While the modulation of miRNAs is emerging as a promising strategy for the regulation of VSMC proliferation, most of the effects of miRNAs and their targets in vivo require further investigation.

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Section: Mirnas Which Inhibit Vsmc Proliferationmentioning

confidence: 99%

Section: Mirnas Which Inhibit Vsmc Proliferationmentioning

confidence: 99%

The microRNAs Regulating Vascular Smooth Muscle Cell Proliferation: A Minireview

Wang

Atanasov

2019

IJMS

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“…The direct target of miR-16 was programmed cell death 4 (PDCD4) [12]. Furthermore, the study of Gu et al [13] also reported lentiviral vector-mediated knockdown of miR-16 promoted Ang II-induced proliferation and migration in vascular smooth muscle cells. Microarray analysis and real-time PCR verified that miR-16 was significantly lower in the CAD patients than that in the non-CAD group [14].…”

Section: Introductionmentioning

confidence: 98%

Overexpression of MicroRNA-16 Alleviates Atherosclerosis by Inhibition of Inflammatory Pathways

Wang

Cai

et al. 2020

BioMed Research International

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Background. Our previous study demonstrated that the expression of miR-16 was downregulated in the cell and animal models of atherosclerosis (AS), a main contributor to coronary artery disease (CAD). Overexpression of miR-16 inhibited the formation of foam cells by exerting anti-inflammatory roles. These findings indicated miR-16 may be an anti-atherogenic and CAD miRNA. The goal of this study was to further validate the expression of miR-16 in CAD patients and explore its therapeutic roles in an AS animal model. Methods. A total of 40 CAD patients and 40 non-CAD people were prospectively registered in our study. The AS model was established in ApoE-/- mice fed a high-fat diet. The model mice were randomly treated with miR-16 agomiR (n=10) or miR-negative control (n=10). Hematoxylin-eosin staining was conducted for histopathological examination in thoracic aorta samples. ELISA and immunohistochemistry were performed to determine the expression levels of inflammatory factors (IL-6, TNF-α, MCP-1, IL-1β, IL-10, and TGF-β). qRT-PCR and western blotting were carried out to detect the mRNA and protein expression levels of PDCD4, miR-16, and mitogen-activated protein kinase pathway-related genes. Results. Compared with the normal control, miR-16 was downregulated in the plasma and peripheral blood mononuclear cell of CAD patients, and its expression level was negatively associated with IL-6 and the severity of CAD evaluated by the Gensini score, but positively related with IL-10. Injection of miR-16 agomiR in ApoE-/- mice reduced the formation of atherosclerotic plaque and suppressed the accumulation of proinflammatory factors (IL-6, TNF-α, MCP-1, and IL-1β) in the plasma and tissues but promoted the secretion of anti-inflammatory factors (IL-10 and TGF-β). Mechanism analysis showed overexpression of miR-16 might downregulate target mRNA PDCD4 and then activate p38 and ERK1/2, but inactivate the JNK pathway. Conclusions. Our findings suggest miR-16 may be a potential diagnostic biomarker and therapeutic target for atherosclerotic CAD.

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“…For instance, miR‐16 represses SALL4 to inhibit the proliferation and migration of gastric cancer cells [ 10 ] ; its silencing promotes the proliferation of vascular smooth muscle cells treated with angiotensin II. [ 11 ] Nevertheless, it is unclear whether miR‐16 plays a role in PAH.…”

Section: Introductionmentioning

confidence: 99%

Docosahexaenoic acid inhibits Ca²⁺ influx and downregulates CaSR by upregulating microRNA‐16 in pulmonary artery smooth muscle cells

Liu

Tang

Zhu

et al. 2020

J Biochem & Molecular Tox

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Docosahexaenoic acid (DHA) is reported to have the potential to ameliorate pulmonary arterial hypertension (PAH), while the specific mechanism is still obscure. This study aims to investigate the function of DHA in pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. In our study, DHA was used to incubate PASMCs. Cytosolic‐free Ca2+ concentration ([Ca2+]cyt) was measured using Fluo‐3 AM method. Real‐time polymerase chain reaction was used to detect microRNA‐16 (miR‐16) and calcium‐sensing receptor (CaSR) messenger RNA expression levels. CCK‐8 assay, BrdU assay, and Transwell assay were employed to detect the effects of DHA on proliferation and migration of PASMCs. CaSR was confirmed as a direct target of miR‐16 using dual‐luciferase assay, polymerase chain reaction, and Western blot analysis. It was found that DHA significantly inhibited PASMC proliferation and migration and decreased [Ca2+]cyt. After transfection of miR‐16 mimics, proliferation and migration ability of PASMCs were significantly inhibited, whereas opposite effects were observed after miR‐16 inhibition. [Ca2+]cyt was also inhibited by miR‐16 transfection. DHA then promoted the expression of miR‐16, and the effects of DHA on PASMCs were annulled when miR‐16 was inhibited. CaSR was identified as a direct target of miR‐16. CaSR was inhibited directly by miR‐16 and indirectly by DHA. In conclusion, DHA inhibits the proliferation and migration of PASMCs, and probably ameliorates PAH via regulating miR‐16/CaSR axis.

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Silencing miR-16 Expression Promotes Angiotensin II Stimulated Vascular Smooth Muscle Cell Growth

Cited by 7 publications

References 34 publications

The microRNAs Regulating Vascular Smooth Muscle Cell Proliferation: A Minireview

The microRNAs Regulating Vascular Smooth Muscle Cell Proliferation: A Minireview

Overexpression of MicroRNA-16 Alleviates Atherosclerosis by Inhibition of Inflammatory Pathways

Docosahexaenoic acid inhibits Ca²⁺ influx and downregulates CaSR by upregulating microRNA‐16 in pulmonary artery smooth muscle cells

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Silencing miR-16 Expression Promotes Angiotensin II Stimulated Vascular Smooth Muscle Cell Growth

Cited by 7 publications

References 34 publications

The microRNAs Regulating Vascular Smooth Muscle Cell Proliferation: A Minireview

The microRNAs Regulating Vascular Smooth Muscle Cell Proliferation: A Minireview

Overexpression of MicroRNA-16 Alleviates Atherosclerosis by Inhibition of Inflammatory Pathways

Docosahexaenoic acid inhibits Ca2+ influx and downregulates CaSR by upregulating microRNA‐16 in pulmonary artery smooth muscle cells

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Docosahexaenoic acid inhibits Ca²⁺ influx and downregulates CaSR by upregulating microRNA‐16 in pulmonary artery smooth muscle cells