miR-223: sailing to terra incognita for microRNAs in platelets

Halkein, Julie; Windt, León J. De

doi:10.1160/th13-10-0882

Cited by 6 publications

(6 citation statements)

References 6 publications

(4 reference statements)

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“…Interestingly, both mature and passenger strands of miR-33 have been shown to affect lipid and even glucose metabolism [19]. Last but not least, miR-223, besides affecting lipid metabolism on the cellular level, is the best example of miR highly abundant in HDL particles [26], microvesicles and exosomes [27] and even platelets [28]. The exact roles of the three abovementioned and other miRs will be described in more detail in this chapter.…”

Section: Micrornas Involvement In Lipid Metabolismmentioning

confidence: 99%

“…Lastly, miR-223 was shown to be involved in platelet function [28] and reactivity to anti-aggregation treatment—in patients with low-response to clopidogrel therapy, platelet miR-223 levels were significantly lower compared to normal-responders [113]. Lower levels of miR-223 were also observed in plasma of low-responders [114]; however, most recently Chyrchel and coworkers presented a study that argues against the notion of low plasma miR-223 as a marker of platelet responsiveness to dual antiplatelet therapy [115].…”

Section: Mir-223: “The Messenger”mentioning

confidence: 99%

See 1 more Smart Citation

Mechanistic Role of MicroRNAs in Coupling Lipid Metabolism and Atherosclerosis

Novák

Olejníčková

Tkáčová

et al. 2015

microRNA: Basic Science

103

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MicroRNAs (miRNAs, miRs) represent a group of powerful and versatile posttranscriptional regulators of gene expression being involved in the fine control of a plethora of physiological and pathological processes. Besides their well-established crucial roles in the regulation of cell cycle, embryogenesis or tumorigenesis, these tiny molecules have also been shown to participate in the regulation of lipid metabolism. In particular, miRs orchestrate cholesterol and fatty acids synthesis, transport, and degradation and low-density and high-density lipoprotein (LDL and HDL) formation. It is thus not surprising that they have also been reported to affect the development and progression of several lipid metabolism-related disorders including liver steatosis and atherosclerosis. Mounting evidence suggests that miRs might represent important “posttranscriptional hubs” of lipid metabolism, which means that one miR usually targets 3′-untranslated regions of various mRNAs that are involved in different steps of one precise metabolic/signaling pathway, e.g., one miR targets mRNAs of enzymes important for cholesterol synthesis, degradation, and transport. Therefore, changes in the levels of one key miR affect various steps of one pathway, which is thereby promoted or inhibited. This makes miRs potent future diagnostic and even therapeutic tools for personalized medicine. Within this chapter, the most prominent microRNAs involved in lipid metabolism, e.g., miR-27a/b, miR-33/33*, miR-122, miR-144, or miR-223, and their intracellular and extracellular functions will be extensively discussed, in particular focusing on their mechanistic role in the pathophysiology of atherosclerosis. Special emphasis will be given on miR-122, the first microRNA currently in clinical trials for the treatment of hepatitis C and on miR-223, the most abundant miR in lipoprotein particles.

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Section: Micrornas Involvement In Lipid Metabolismmentioning

confidence: 99%

Section: Mir-223: “The Messenger”mentioning

confidence: 99%

Mechanistic Role of MicroRNAs in Coupling Lipid Metabolism and Atherosclerosis

Novák

Olejníčková

Tkáčová

et al. 2015

microRNA: Basic Science

103

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“…This result is of special interest, as platelets contain high levels of miR‐223 and are a major source of plasma miR‐223 . In this sense, Halken and De Windt hypothesized that certain platelet miRNAs ‘may act in target cells other than the ones where they are produced', a proposal that deserves deeper research . Actually, a report published a short time later showed that platelet microvesicles formed after thrombopoietin or thrombin activation contain high levels of miR‐223 that are able to induce the formation of advanced glycation end‐products, inducing human umbilical vein enothelial cell (HUVEC) apoptosis by targeting insulin‐like growth factor 1 receptor .…”

Section: Mirna As a Regulator Of The Hemostatic Systemmentioning

confidence: 99%

MicroRNAs in hemostasis

Teruel‐Montoya

Rosendaal

Martı́nez

2015

Journal of Thrombosis and Haemostasis

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To cite this article: Teruel-Montoya R, Rosendaal FR, Mart ınez C. MicroRNAs in hemostasis. J Thromb Haemost 2015; 13: 170-81.Summary. Epidemiologic studies have revealed that modification of the levels of individual components of the hemostatic system may have effects on the development of thrombosis or hemorrhage. To maintain the necessary equilibrium, the hemostatic system is finely regulated. It is known that acquired factors and/or alterations in genes (single-nucleotide polymorphisms or mutations) may be the cause of interindividual differences or exacerbated levels of hemostatic proteins in plasma, but there are still many non-characterized factors that provoke such variations. The search for new elements, such as microRNAs (miRNAs), a family of small non-coding RNAs that are novel regulators of protein expression, may reveal an additional layer at which to investigate the causes of hemostatic diseases. In this review, we discuss the latest developments in research into the role of miRNAs in the regulation of several hemostatic factors, and the potential use of miRNAs as prognostic or diagnostic tools in hemostasis and thrombosis.

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“…A number of highly expressed miRNA have been characterised in human platelets, some of which are involved in myeloid cell differentiation, megakaryocytopoiesis and thrombopoiesis. miR-223 has been identified as the most highly expressed platelet miRNA [38,43,44] and has roles in thrombopoiesis and megakaryocyte differentiation [24]. miR-223 regulates ADP P2Y 12 , a target for existing anti-platelet drug therapy.…”

Section: Platelet Epigenetics 21 Platelet Mirnamentioning

confidence: 99%

Platelets: Functional Biomarkers of Epigenetic Drift

Twomey¹,

Wallace²,

Mangone³

et al. 2019

Homeostasis - An Integrated Vision

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Cardiovascular disease (CVD) risk factors can be classed as modifiable or non-modifiable. Physical inactivity and obesity represent major behavioural risk factors for the initiation, development and progression of CVD. Platelet dysfunction is pivotal to the aetiology of CVD, a chronic vascular inflammatory condition, which is characterised by a lag time between onset and clinical manifestation. This indicates the role of epigenetic drift, defined by stochastic patterns of gene expression not dependent on dynamic changes in coding DNA. The epigenome, a collection of chemical marks on DNA and histones, is established during embryogenesis and modified by age and lifestyle. Biogenesis and effector function of non-coding RNA, such as microRNA, play a regulatory role in gene expression and thus the epigenetic mechanism. In this chapter, we will focus on the effect of the modifiable risk factors of physical activity/inactivity and overweight/obesity on platelet function, via epigenetic changes in both megakaryocytopoiesis and thrombopoiesis. We will also discuss the role of acute exercise on platelet function and the impact of cardiorespiratory fitness (CRF) on platelet responses to acute exercise. This chapter will highlight the potential role of platelets as circulating functional biomarkers of epigenetic drift to implement, optimise and monitor CVD preventive management strategies.

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miR-223: sailing to terra incognita for microRNAs in platelets

Abstract: Insight miR-223 plays a remarkably modest role in thrombopoiesis and platelet function does not depend upon miR-223

Cited by 6 publications

References 6 publications

Mechanistic Role of MicroRNAs in Coupling Lipid Metabolism and Atherosclerosis

Mechanistic Role of MicroRNAs in Coupling Lipid Metabolism and Atherosclerosis

MicroRNAs in hemostasis

Platelets: Functional Biomarkers of Epigenetic Drift

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