MicroRNA-223 inhibits tissue factor expression in vascular endothelial cells

Li, Sufang; Chen, Hong; Ren, Jingyi; Geng, Qiang; Song, Junxian; Lee, Chongyou; Cao, Chao; Zhang, Jing; Xu, Ning

doi:10.1016/j.atherosclerosis.2014.09.033

Cited by 73 publications

(44 citation statements)

References 32 publications

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“…Role of miRNAs in regulation of TF and arterial thrombosis has only recently begun to emerge. For example, miR-223 and miR-19 inhibit TF expression in ECs (33)(34)(35). In the current study, we found that miR-181b inhibits TF expression in thrombintreated ECs.…”

Section: Discussionsupporting

confidence: 60%

MicroRNA‐181b inhibits thrombin‐mediated endothelial activation and arterial thrombosis by targeting caspase recruitment domain family member 10

Lin

Sun

et al. 2016

FASEB j.

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Thrombogenic and inflammatory mediators, such as thrombin, induce NF-kB-mediated endothelial cell (EC) activation and dysfunction, which contribute to pathogenesis of arterial thrombosis. The role of anti-inflammatory microRNA-181b (miR-181b) on thrombosis remains unknown. Our previous study demonstrated that miR-181b inhibits downstream NF-kB signaling in response to TNF-a. Here, we demonstrate that miR-181b uniquely inhibits upstream NF-kB signaling in response to thrombin. Overexpression of miR-181b inhibited thrombin-induced activation of NF-kB signaling, demonstrated by reduction of phospho-IKK-b, -IkB-a, and p65 nuclear translocation in ECs. MiR-181b also reduced expression of NF-kB target genes VCAM-1, intercellular adhesion molecule-1, E-selectin, and tissue factor. Mechanistically, miR-181b targets caspase recruitment domain family member 10 (Card10), an adaptor protein that participates in activation of the IKK complex in response to signals transduced from protease-activated receptor-1. miR-181b reduced expression of Card10 mRNA and protein, but not protease-activated receptor-1. 39-Untranslated region reporter assays, argonaute-2 microribonucleoprotein immunoprecipitation studies, and Card10 rescue studies revealed that Card10 is a bona fide direct miR-181b target. Small interfering RNA-mediated knockdown of Card10 expression phenocopied effects of miR-181b on NF-kB signaling and targets. Card10 deficiency did not affect TNF-a-induced activation of NF-kB signaling, which suggested stimulus-specific regulation of NF-kB signaling and endothelial responses by miR-181b in ECs. Finally, in response to photochemical injuryinduced arterial thrombosis, systemic delivery of miR-181b reduced thrombus formation by 73% in carotid arteries and prolonged time to occlusion by 1.6-fold, effects recapitulated by Card10 small interfering RNA. These data demonstrate that miR-181b and Card10 are important regulators of thrombin-induced EC activation and arterial thrombosis. These studies highlight the relevance of microRNA-dependent targets in response to ligand-specific signaling in

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Section: Discussionsupporting

confidence: 60%

MicroRNA‐181b inhibits thrombin‐mediated endothelial activation and arterial thrombosis by targeting caspase recruitment domain family member 10

Lin

Sun

et al. 2016

FASEB j.

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“…Evidence is emerging suggesting that TNF-α may affect vascular cell functions by modulating the expression of different miRNA molecules [42, 43]. Consistent with our present results, Wei et al .…”

Section: Discussionsupporting

confidence: 93%

Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation

et al. 2017

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In this study, we tested the possibility that macrophages might contribute to neointima formation by stimulating microRNA expressions in mural cells. Thoracic aortas from F344 rats were transplanted into recipient Lewis rats. Clodronate liposome was used for in vivo macrophage depletion. Using miR-21 as a prototypic example of vascular enriched microRNA, we showed that macrophage depletion reduced the expression level of miR-21, which was upregulated in the allograft. This effect of macrophage depletion was accompanied by attenuations in neointimal hyperplasia and transplantation-induced vascular inflammation. Using in vitro assays, we identified that macrophages might stimulate miR-21 expression in smooth muscle cells and adventitial fibroblasts via the release of tumor necrosis factor-α. We also showed that silencing of miR-21 suppressed tumor necrosis factor-induced proliferation, migration, and inflammatory responses in mural cells. Our results suggest that macrophage may promote transplantation-induced neointima formation by stimulating miR-21 expression in vascular mural cells, which promotes mural cell proliferation, migration and/or inflammation. Moreover, we have established that tumor necrosis factor-α has a major role in mediating this paracrine process.

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“…TF expression by endothelium has been associated with the occurrence of thrombotic events in patients with a variety of clinical disorders including atherosclerosis [68]. The proinflammatory microenvironment characteristic of human atherosclerotic plaque induces the production of TF by various cell types including ECs, vascular smooth muscle cells, and monocytes [69]. If the atherosclerotic lesion undergoes rupture, TF is released into the bloodstream [70, 71] and activates the coagulation pathway, thus promoting thrombotic events [72].…”

Section: Discussionmentioning

confidence: 99%

The Nutraceutical Dehydrozingerone and Its Dimer Counteract Inflammation‐ and Oxidative Stress‐Induced Dysfunction of In Vitro Cultured Human Endothelial Cells: A Novel Perspective for the Prevention and Therapy of Atherosclerosis

Profumo

Buttari

D’Arcangelo

et al. 2016

Oxidative Medicine and Cellular Longevity

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Atherosclerosis is characterized by endothelial dysfunction, mainly induced by inflammation and oxidative stress. Increased reactive oxygen species (ROS) production together with increased adhesion molecules and thrombogenic tissue factor (TF) expression on endothelial cells has a key role in proatherogenic mechanisms. Therefore downmodulation of these molecules could be useful for reducing the severity of inflammation and atherosclerosis progression. Dehydrozingerone (DHZ) is a nutraceutical compound with anti-inflammatory and antioxidant activities. In this study we evaluated the ability of DHZ and its symmetric dimer to modulate hydrogen peroxide- (H2O2-) induced ROS production in human umbilical vein endothelial cells (HUVEC). We also evaluated intercellular adhesion molecule- (ICAM-) 1, vascular cell adhesion molecule- (VCAM-) 1, and TF expression in HUVEC activated by tumor necrosis factor- (TNF-) α. HUVEC pretreatment with DHZ and DHZ dimer reduced H2O2-induced ROS production and inhibited adhesion molecule expression and secretion. Of note, only DHZ dimer was able to reduce TF expression. DHZ effects were in part mediated by the inhibition of the nuclear factor- (NF-) κB activation. Overall, our findings demonstrate that the DHZ dimer exerts a potent anti-inflammatory, antioxidant, and antithrombotic activity on endothelial cells and suggest potential usefulness of this compound to contrast the pathogenic mechanisms involved in atherosclerosis progression.

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MicroRNA-223 inhibits tissue factor expression in vascular endothelial cells

Cited by 73 publications

References 32 publications

MicroRNA‐181b inhibits thrombin‐mediated endothelial activation and arterial thrombosis by targeting caspase recruitment domain family member 10

MicroRNA‐181b inhibits thrombin‐mediated endothelial activation and arterial thrombosis by targeting caspase recruitment domain family member 10

Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation

The Nutraceutical Dehydrozingerone and Its Dimer Counteract Inflammation‐ and Oxidative Stress‐Induced Dysfunction of In Vitro Cultured Human Endothelial Cells: A Novel Perspective for the Prevention and Therapy of Atherosclerosis

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