MicroRNA Regulation of Angiogenesis and Arteriogenesis

Hans, Felix Patricius; Moser, Martin; Bode, Christoph; Grundmann, Sebastian

doi:10.1016/j.tcm.2011.12.001

Cited by 19 publications

(16 citation statements)

References 71 publications

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“…It had been found that there is the close relationship between miR-146a and angiogenesis [7]. Our data are consistent with this earlier finding because we discovered that the level of miR-146a is increased in CAD patients with good CCC and decreased in those with poor CCC.…”

Section: Discussionsupporting

confidence: 93%

“…It has been reported that miR-146a can exert proangiogenic effects [7] and can upregulate VEGF-A [11], which is one of the most important vascular growth factors during angiogenesis. In this study, we measured levels of plasma VEGF-A and miR-146a in patients that had been classified by their CCC status.…”

Section: Resultsmentioning

confidence: 99%

“…It has been established that miRNAs function as key regulators of different aspects of vascular biology, including angiogenesis [6]. It has been reported that there is a close relationship between angiogenesis and several miRNAs: miR-21, miR-146a, miR-155, miR-221, and miR-222 [7]. All of these have been shown to exert antiangiogenic effects, apart from miR-146a [7].…”

Section: Introductionmentioning

confidence: 99%

“…It has been reported that there is a close relationship between angiogenesis and several miRNAs: miR-21, miR-146a, miR-155, miR-221, and miR-222 [7]. All of these have been shown to exert antiangiogenic effects, apart from miR-146a [7]. Although angiogenesis plays an important role in CCC formation [8], the correlation between miR-146a and the CCC has not been substantially investigated.…”

Section: Introductionmentioning

confidence: 99%

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Reduced Plasma miR-146a Is a Predictor of Poor Coronary Collateral Circulation in Patients with Coronary Artery Disease

Wang

Yan

Song

et al. 2016

BioMed Research International

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Coronary collateral circulation (CCC), an alternative blood supply for ischemic myocardium, improves survival rates among patients with coronary artery disease (CAD). However, there remains a lack of biomarkers to discriminate between patients with poor or good CCC. In this study, we aimed to observe the relationship between plasma microRNA-146a (miR-146a) levels and the coronary collateral circulation (CCC). Additionally, we aimed to explore whether the plasma miR-146a level could serve as a blood-based biomarker for CCC in patients with CAD. We measured the plasma levels of vascular endothelial growth factor A (VEGF-A) and miR-146a in patients with CCC by ELISA and real-time PCR, respectively, according to the Rentrop grades. The results showed that the plasma miR-146a level is significantly increased in CAD patients with good CCC and significantly decreased in those with poor CCC. In contrast, although VEGFA expression in patients followed a similar trend as the CCC, the differences between the groups were not statistically significant. There was a positive correlation between plasma miR-146a levels and the Rentrop grading. In addition, receiver operator characteristic analysis showed that miR-146a could be a potent biomarker for identifying patients with poor CCC.

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Section: Discussionsupporting

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Reduced Plasma miR-146a Is a Predictor of Poor Coronary Collateral Circulation in Patients with Coronary Artery Disease

Wang

Yan

Song

et al. 2016

BioMed Research International

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“…22 Although miR-155 may not be an ideal therapeutic target, the identification of others miRNAs that promote neovascularization could lead to novel miRNA-based therapies that are specific to arteriogenesis and do not activate inflammation, avoiding many of the resultant confounders. 23 The molecular regulators of arteriogenesis continue to emerge, and we can now add macrophage miR-155 to the list. Although therapies that promote the growth of collateral arteries to revascularize and repair the myocardium continue to be elusive, many clinical trials in this area are focused on either delivery of cardiac progenitor cells to the site of injury or delivery of factors that promote the recruitment of progenitor cells from the bone marrow, with the hope that these cells will differentiate into new vascular endothelium or myocardium.…”

Section: Article See P 1575mentioning

confidence: 99%

MicroRNA-155 in the Heart

Rayner

2015

Circulation

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MicroRNA‐384‐3p inhibits retinal neovascularization through targeting hexokinase 2 in mice with diabetic retinopathy

Xia

Sun

Jiang

et al. 2018

Journal Cellular Physiology

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Diabetic retinopathy (DR) presents a microvascular complication of diabetes, which may contribute to visual impairment. The treatment of DR is still controversial. Accumulating studies have reported the role of microRNAs (miRs) in DR. This study aims to explore the functions of microRNA-384-3p (miR-384-3p) in retinal neovascularization by targeting hexokinase 2 (HK2) in mice with DR. A total of 43 C57BL/6 male mice were selected and divided into normal ( n = 16) and DR ( n = 27) groups. Retinal microvascular endothelial cells (RMECs) were collected from the normal and DR mice and mainly treated with a miR-384-3p mimic, a miR-384-3p inhibitor, small interfering RNA (siRNA) against HK2 and HK2 overexpression plasmids to understand the underlying regulatory mechanisms of miR-384-3p. The relationship between miR-384-3p and HK2 was determined by dual-luciferase reporter assay. The miR-384-3p expression and the mRNA and the protein expressions of HK2 and CD31 in retinal tissues and cells were evaluated using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot assay. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Tube formation was observed by conducting a tube formation experiment. HK2 is a target gene of miR-384-3p. The DR mice showed higher expression of HK2 and CD31 but lower expression of miR-384-3p. The miR-384-3p mimic and siRNA-HK2 reduced the expression of HK2, decreased cell proliferation and tube formation of RMECs, whereas the miR-384-3p inhibitor could reverse these trends. Our study demonstrates that overexpression of miR-384-3p inhibits retinal neovascularization in DR mice via inhibition of HK2.

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MicroRNA Regulation of Angiogenesis and Arteriogenesis

Cited by 19 publications

References 71 publications

Reduced Plasma miR-146a Is a Predictor of Poor Coronary Collateral Circulation in Patients with Coronary Artery Disease

Reduced Plasma miR-146a Is a Predictor of Poor Coronary Collateral Circulation in Patients with Coronary Artery Disease

MicroRNA-155 in the Heart

MicroRNA‐384‐3p inhibits retinal neovascularization through targeting hexokinase 2 in mice with diabetic retinopathy

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