MicroRNA-126 modulates endothelial SDF-1 expression and mobilization of Sca-1+/Lin− progenitor cells in ischaemia

Solingen, Coen van; Boer, Hetty C. de; Bijkerk, Roel; Monge, Matthieu; Oeveren‐Rietdijk, Annemarie M. van; Seghers, Leonard; Vries, Margreet R. de; Veer, Eric P. van der; Quax, Paul H.A.; Rabelink, Ton J.; Zonneveld, Anton Jan van

doi:10.1093/cvr/cvr227

Cited by 85 publications

(54 citation statements)

References 43 publications

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“…In addition, Harris et al [28] reported that miR-126-5p negatively regulates leukocyte adherence to ECs by targeting endothelial vascular cell adhesion molecule-1 (VCAM-1) in ECs. A study by Van Solingen et al showed that transferring ECderived apoptotic micro-vesicles containing miR-126-5p into atherosclerotic lesions significantly ameliorates the progression of atherosclerosis through the recruitment of Sca-1-positive EC progenitor cells [29]. Meanwhile, miR-126-5p also could promote endothelial proliferation and limit atherosclerosis by suppressing Notch1 inhibitor delta-like 1 homolog (Dlk1) [30].…”

Section: Discussionmentioning

confidence: 99%

Plasma MicroRNA-126-5p is Associated with the Complexity and Severity of Coronary Artery Disease in Patients with Stable Angina Pectoris

Zhao

Liu

et al. 2016

Cell Physiol Biochem

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Background: Coronary artery disease (CAD) is a major problem worldwide. As an endothelium-enriched microRNA (miRNA), miR-126 has been reported to serve as a potential biomarker of acute myocardial infarction. However, the relationship between miR-126 and the severity of CAD remains unknown. This study was designed to test whether circulating miR-126 levels are associated with the severity of CAD. Methods: The present study enrolled 40 patients who had risk factors for CAD without angiographically significant CAD, and 110 patients presenting with stable angina pectoris, who were validated left main coronary artery disease (LMCA) and/or multi-vessel disease by coronary angiography. The expression levels of plasma miR-126-5p from all enrolled subjects were estimated by quantitative real-time polymerase chain reaction (qRT-PCR). Then, the relationships between plasma miR-126-5p levels, number of diseased vessels and the corresponding Synergy between PCI with Taxus and Cardiac surgery (SYNTAX) score were analyzed. Results: The expression of circulating miR-126-5p was affected by some CAD risk factors including aging, dyslipidemia and DM. Furthermore, plasma miR-126-5p levels were significantly down-regulated in CAD patients with multi-vessel disease, higher SYNTAX score, rather than isolated LMCA and low SYNTAX score. Conclusion: Circulating miR-126-5p has emerged as a potential biomarker for complexity and severity of CAD in patients with stable angina pectoris.

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Section: Discussionmentioning

confidence: 99%

Plasma MicroRNA-126-5p is Associated with the Complexity and Severity of Coronary Artery Disease in Patients with Stable Angina Pectoris

Zhao

Liu

et al. 2016

Cell Physiol Biochem

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“…In extant studies, chemokine signaling mediated by Cxcl12a was reported to guide lymphangioblast extension along HM to form the PL during trunk lymphatic development, 15 and human Cxcl12 (SDF-1 [stromal cell-derived factor-1]) was identified as a miR-126 target. 31, 32 We thus reasoned that Cxcl12a would be a target of miR-126a in zebrafish. Using bioinformatics analysis, zebrafish Cxcl12a mRNA 3′ UTR was not predicted to be a target of miR-126a, and the result of in vivo GFP reporter assay further indicated that miR-126a did not bind to zebrafish Cxcl12a mRNA's 3′ UTR (Figure VIB through VID in the online-only Data Supplement).…”

Section: Cxcl12a Is a Direct Target Of Mir-126a Through Post-transcrimentioning

confidence: 99%

MicroRNA-126a Directs Lymphangiogenesis Through Interacting With Chemokine and Flt4 Signaling in Zebrafish

Chen

Zhu

et al. 2016

ATVB

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Objective— MicroRNA-126 (miR-126) is an endothelium-enriched miRNA and functions in vascular integrity and angiogenesis. The application of miRNA as potential biomarker and therapy target has been widely investigated in various pathological processes. However, its role in lymphatic diseases had not been widely explored. We aimed to reveal the role of miR-126 in lymphangiogenesis and the regulatory signaling pathways for potential targets of therapy. Approach and Results— Loss-of-function studies using morpholino oligonucleotides and CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9) system showed that silencing of miR-126a severely affected the formation of parachordal lymphangioblasts and thoracic duct in zebrafish embryos, although their development in miR-126b knockdown embryos was normal. Expression analyses by in situ hybridization and immunofluorescence indicated that miR-126a was expressed in lymphatic vessels, as well as in blood vessels. Time-lapse confocal imaging assay further revealed that knockdown of miR-126a blocked both lymphangiogenic sprouts budding from the posterior cardinal vein and lymphangioblasts extension along horizontal myoseptum. Bioinformatics analysis and in vivo report assay identified that miR-126a upregulated Cxcl12a by targeting its 5′ untranslated region. Moreover, loss- and gain-of-function studies revealed that Cxcl12a signaling acted downstream of miR-126a during parachordal lymphangioblast extension, whereby Flt4 signaling acts as a cooperator of miR-126a, allowing it to modulate lymphangiogenic sprout formation. Conclusions— These findings demonstrate that miR-126a directs lymphatic endothelial cell sprouting and extension by interacting with Cxcl12a-mediated chemokine signaling and Vegfc-Flt4 signal axis. Our results suggest that these key regulators of lymphangiogenesis may be involved in lymphatic pathogenesis of cardiovascular diseases.

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“…60 Additionally, miR-126 in ECs regulates vascular remodeling by modulating the expression of stromal cellderived factor-1 (SDF-1). 61 In vivo, elevated levels of SDF-1 were proposed to mediate the recruitment and mobilization of Sca-1ϩ/Lin-progenitor cells to the ischemic region.…”

Section: Mir-126 As Master Regulator Of Endothelial Functionmentioning

confidence: 99%

MicroRNAs in Vascular and Metabolic Disease

Zampetaki

Mayr

2012

Circulation Research

227

170

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They are potent modulators of diverse biological processes and pathologies comprising 1-5% of mammalian genes. 1,2 Recently, distinct miRNA signatures have been reported in cardiovascular disease 3,4 and miRNAs are implicated as targets for therapeutic interventions. 5 Intriguingly, miRNAs emerged as key regulators of established cardiovascular risk factors, such as diabetes, hypercholesterolemia, and so forth. 6 We review the role of miRNAs in vascular and metabolic diseases and the contribution of -omics technologies to further our understanding of miRNA function and their mechanisms of action. MiRNAs as Regulators of Metabolic PathwaysAnimal models and genetic studies have highlighted the prominent role of miRNAs in the regulation of lipid metabolism (Figure 1). MiRNAs also safeguard insulin expression Original

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MicroRNA-126 modulates endothelial SDF-1 expression and mobilization of Sca-1+/Lin− progenitor cells in ischaemia

Cited by 85 publications

References 43 publications

Plasma MicroRNA-126-5p is Associated with the Complexity and Severity of Coronary Artery Disease in Patients with Stable Angina Pectoris

Plasma MicroRNA-126-5p is Associated with the Complexity and Severity of Coronary Artery Disease in Patients with Stable Angina Pectoris

MicroRNA-126a Directs Lymphangiogenesis Through Interacting With Chemokine and Flt4 Signaling in Zebrafish

MicroRNAs in Vascular and Metabolic Disease

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