Cardiovascular inflammation: RNA takes the lead

Martens, Colton R.; Bansal, Shyam S.; Accornero, Federica

doi:10.1016/j.yjmcc.2019.03.012

Cited by 20 publications

(15 citation statements)

References 145 publications

(175 reference statements)

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“…In a study by Vickers et al, miR-222 level in circulating HDL was found to be 8.2-fold higher in familial hypercholesterolemia patients compared with HDL from normal subjects 64) . miR-222 regulates insulin sensitivity, and miR-222 levels are higher in plasma of obese human patients 70) .…”

Section: Shear Stress-induced Pcsk9 Expressionmentioning

confidence: 91%

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An Update on the Role of PCSK9 in Atherosclerosis

Yurtseven

Ural

Baysal

et al. 2020

JAT

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The official journal of the Japan Atherosclerosis Society and the Asian Pacific Society of Atherosclerosis and Vascular Diseases Review Atherosclerosis is initiated by functional changes in the endothelium accompanied by accumulation, oxidation, and glycation of LDL-cholesterol in the inner layer of the arterial wall and continues with the expression of adhesion molecules and release of chemoattractants. PCSK9 is a proprotein convertase that increases circulating LDL levels by directing hepatic LDL receptors into lysosomes for degradation. The effects of PCSK9 on hepatic LDL receptors and contribution to atherosclerosis via the induction of hyperlipidemia are well defined. Monoclonal PCSK9 antibodies that block the effects of PCSK9 on LDL receptors demonstrated beneficial results in cardiovascular outcome trials. In recent years, extrahepatic functions of PCSK9, particularly its direct effects on atherosclerotic plaques have received increasing attention. Experimental trials have revealed that PCSK9 plays a significant role in every step of atherosclerotic plaque formation. It contributes to foam cell formation by increasing the uptake of LDL by macrophages via scavenger receptors and inhibiting cholesterol efflux from macrophages. It induces the expression of inflammatory cytokines, adhesion molecules, and chemoattractants, thereby increasing monocyte recruitment, inflammatory cell adhesion, and inflammation at the atherosclerotic vascular wall. Moreover, low shear stress is associated with increased PCSK9 expression. PCSK9 may induce endothelial cell apoptosis and autophagy and stimulate the differentiation of smooth muscle cells from the contractile phenotype to synthetic phenotype. Increasing evidence indicates that PCSK9 is a molecular target in the development of novel approaches toward the prevention and treatment of atherosclerosis. This review focuses on the molecular roles of PCSK9 in atherosclerotic plaque formation.

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Section: Shear Stress-induced Pcsk9 Expressionmentioning

confidence: 91%

“…To clarify its role in atherosclerosis and its reason for existence, further research is required. production 63,64) .…”

Section: Shear Stress-induced Pcsk9 Expressionmentioning

confidence: 99%

An Update on the Role of PCSK9 in Atherosclerosis

Yurtseven

Ural

Baysal

et al. 2020

JAT

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“…MicroRNAs affect gene expression, and their dysregulation increases inflammation and leads to atherosclerosis [11][12][13]. Studies have shown that many microRNAs, including miR-504, -200, -138 and -210, regulate the proliferation and migration of VSMCs [3].…”

Section: Introductionmentioning

confidence: 99%

Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration

Zhou

Ran

et al. 2020

Aging

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We investigated the protective effects and mechanism of action of metformin on high glucose-induced smooth muscle cell proliferation and migration. Vascular smooth muscle cells (VSMCs) were subjected to a series of concentrations (0-10 mM) of metformin. CCK-8, wound healing, and transwell assays were performed. Correlations between metformin concentration and high-mobility group box 1 (HMGB1) and miR-142-3p levels were assessed. In addition, miR-142-3p mimic and siRNA were used to investigate VSMC migration in the presence or absence of metformin. In the high-glucose condition, metformin decreased cell growth and inhibited cell migration. HMGB1 gene expression correlated negatively with metformin concentration, whereas miR-142-3p expression correlated positively with metformin concentration. In addition, mimic-induced miR-142-3p elevation resulted in decreased HMGB1 and LC3II levels and elevated p62 levels in the high-glucose condition, whereas miR-142-3p knockdown had the reverse effects, and metformin abolished those effects. Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway.

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“…In deed, the regulation of miRNAs with specific genes in cells can modulate specific biological pathways. The extensive dysregulation of miRNA expression may reflect multiple cellular defense responses caused by inflammation, bacterial infections, and viral infections [34][35][36]. Upon viral infection, the host can alter several specific biological pathways, such as differentiated growth, development, apoptosis, changes in metabolic pathway, and homeostasis.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA 876-5p modulates EV-A71 replication through downregulation of host antiviral factors

Cheng

et al. 2020

Virol J

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Background: Human enterovirus 71 (EV-A71) is a non-enveloped virus that has a single stranded positive sense RNA genome. In a previous study, we showed that miR-876-5p upregulation was observed in the serum of patients with severe EV-A71 infection. Micro-876-5p (miR-876-5p) is a circulating miRNA that can be identified to modulate EV-A71 infections through both in vitro and in vivo studies. However, the regulatory mechanisms that involve miR-876-5p in the EV-A71 infection cycle remain unclear. Methods: We demonstrated that miR-876-5p facilitated EV-A71 replication and expression by overexpression and knocking-down of miR-876-5p through the transfection of miR-876-5p plasmid and miR-876-5p inhibitor. Although miR-876-5p suppressed CREB5 expression, luciferase reporter assay confirmed this. We also evaluated the role of miR-876-5p in the EV-A71 infection cycle by CREB5 mediated by transfection with an anti-miR-876-5P inhibitor or in combination with an si-CREB5 plasmid. Results: MicroR-876-5p was upregulated in EV-A71-infected neuroblastoma cells. Overexpression of miR-876-5p or knockdown of cyclic-AMP responsive element binding protein 5 (CREB5) promoted EV-A71 replication. The downregulation of miR-876-5p inhibited the accumulation of viral RNA and the production of viral proteins. Interestingly, CREB5 overexpression also suppressed EV-A71 replication. Our in vitro studies reveal that miR-876-5p directly targets CREB5. Finally, downregulation of CREB5 protein abated the inhibitory effect of anti-miR-876-5p and induced inhibitory effect of EV-A71 replication. Conclusions: Our results suggest that intracellular miR-876-5p promotes EV-A71 replication indirectly by targeting the host CREB5 protein.

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Cardiovascular inflammation: RNA takes the lead

Cited by 20 publications

References 145 publications

An Update on the Role of PCSK9 in Atherosclerosis

An Update on the Role of PCSK9 in Atherosclerosis

Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration

MicroRNA 876-5p modulates EV-A71 replication through downregulation of host antiviral factors

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