MicroRNA-223 coordinates cholesterol homeostasis

Vickers, KC; Landstreet,; Levin, Michael G.; Shoucri, BM; Toth, CL; Rc, Taylor; Palmisano, Brian T.; Tabet, Fatiha; Cui, H. L.; Rye, K.-A.; Sethupathy, Praveen; Remaley, A.T.

doi:10.1073/pnas.1215767111

Cited by 226 publications

(239 citation statements)

References 46 publications

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“…9, 10 Interestingly, miR-223 has been described to be a post-transcriptional regulator of various aspects of cholesterol metabolism; miR-223 represses the SR-BI-mediated selective uptake of cholesteryl esters from HDL and cholesterol biosynthesis and by increasing ABCA1 expression promotes cholesterol efflux towards apoA-I. 120 HDL was shown to deliver miR-223 into endothelial cells, where it downregulates expression of intracellular cell adhesion molecule 1 (ICAM-1). 121 However, these findings are in contrast to those by Wagner et al 10 who confirmed the presence of low copy numbers of miRNAs in HDL, but found no evidence that HDL delivers physiologically relevant amounts of miRNAs into endothelial cells, smooth muscle cells, and peripheral blood mononuclear cells.…”

Section: Sphingolipidsmentioning

confidence: 99%

Dysfunctional high-density lipoproteins in coronary heart disease: implications for diagnostics and therapy

Annema

Eckardstein

2016

Translational Research

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Low plasma levels of high-density lipoprotein (HDL) cholesterol are associated with increased risks of coronary heart disease. HDL mediates cholesterol efflux from macrophages for reverse transport to the liver and elicits many anti-inflammatory and anti-oxidative activities which are potentially antiatherogenic. Nevertheless, HDL has not been successfully targeted by drugs for prevention or treatment of cardiovascular diseases. One potential reason is the targeting of HDL cholesterol which does not capture the structural and functional complexity of HDL particles. Hundreds of lipid species and dozens of proteins as well as several microRNAs have been identified in HDL. This physiological heterogeneity is further increased in pathologic conditions due to additional quantitative and qualitative molecular changes of HDL components which have been associated with both loss of physiological function and gain of pathologic dysfunction. This structural and functional complexity of HDL has prevented clear assignments of molecules to the functions of normal HDL and dysfunctions of pathologic HDL. Systematic analyses of structure-function relationships of HDL-associated molecules and their modifications are needed to test the different components and functions of HDL for their relative contribution in the pathogenesis of atherosclerosis. The derived biomarkers and targets may eventually help to exploit HDL for treatment and diagnostics of cardiovascular diseases.

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Section: Sphingolipidsmentioning

confidence: 99%

Dysfunctional high-density lipoproteins in coronary heart disease: implications for diagnostics and therapy

Annema

Eckardstein

2016

Translational Research

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“…4,5 A recent study reports that miR-223 also coordinates cholesterol homeostasis. 6 In the liver, the expression of miR-223 is increased during ischemic and reperfusion injury. 7 miR-223 in hepatic macrophages (Kupffer cells) has been shown to inhibit IL-1b production and thus suppress proinflammatory response during concanavalin Aeinduced acute liver injury.…”

mentioning

confidence: 99%

miR-223 Deficiency Protects against Fas-Induced Hepatocyte Apoptosis and Liver Injury through Targeting Insulin-Like Growth Factor 1 Receptor

Qadir

Chen

Chang

et al. 2015

The American Journal of Pathology

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The biological functions and molecular mechanisms of miR-223 action in liver cells and liver diseases remain unclear. We therefore determined the effect and mechanism of action of miR-233 in Fas-induced hepatocyte apoptosis and liver injury. Wild-type (WT) and miR-223 knockout (KO) mice were treated i.p. with 0.5 mg/g body weight anti-Fas antibody Jo2, and the animals were monitored for survival and the extent of liver injury. Although WT mice died 4 to 6 hours after Jo2 injection (n Z 6), all of the miR-223 KO mice (n Z 6) survived. In comparison to WT mice, the miR-223 KO mice showed resistance to Fas-induced liver injury, as indicated by less tissue damage under histopathological examination, fewer apoptotic hepatocytes under caspase-3 immunostaining, and less elevation of serum transaminases. miR-223 KO livers showed less caspase-3, caspase-8, and caspase-9 activation and less poly (ADP-ribose) polymerase cleavage compared with WT livers (P < 0.05). Furthermore, tail vein injection of miR-223 lentiviral vector to miR-223 KO mice restored Jo2-induced liver injury. Transfection of miR-223 KO hepatocytes with miR-223 mimic enhanced Jo2-induced activation of caspase-3, caspase-8, and caspase-9, whereas transfection of WT hepatocytes with the miR-223 inhibitor attenuated Jo2-induced apoptosis. These findings demonstrate that miR-223 deficiency protects against Fas-induced hepatocyte apoptosis and liver injury. Further in vitro and in vivo data indicate that miR-223 regulates Fas-induced hepatocyte apoptosis and liver injury by targeting the insulin-like growth factor 1 receptor. (Am J Pathol 2015, 185: 3141e3151; http://dx

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“…Moreover, miR-221 and miR-222 have been shown to control other miRNAs, particularly miR-223. It was reported that platelets of patients with atherosclerosis displayed increased miR-223, which participated in cholesterol biosynthesis, and was considered to be a potential mediator in the pathogenesis of atherosclerosis [31]. On the other hand, the angiogenesis-related miRNA-106b, -25, -92a and -21 levels were also demonstrated to increase in the atherosclerotic plaque [32].…”

Section: Micro-rnas In Cardiovascular Diseasesmentioning

confidence: 99%

Unknown Aspects of Well-known Cardiovascular Diseases: Identification of Novel miRNA Genes

Çeviker¹,

Bağcı²,

Yazkan³

2016

Ann Clin Anal Med

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ÖzetKodlanmayan küçük ribonükleik asit (miRNA)'lerin bulunması ve işlevlerinin tanımlanmasıyla, RNA'ların canlı yaşamı için çok önemli süreçlerde rol oynadıkları belirlenmiştir. miRNA'larda meydana gelen bozukluklar birçok hastalı-ğa yol açmaktadır. Beklendiği üzere kanserler, nörodejeneratif hastalıklar ve immün yetmezlik gibi hastalıklarla ilişkilendirilmiş ve son yıllarda yeni yapı-lan çalışmalarla kardiyovasküler hastalıklarla olan ilişkilileri gösterilmiştir. Bu miRNA'lar, yeni tedavi yaklaşımlarında hem hedef hem de araç olarak görül-mektedirler. İnsan genomundaki tüm miRNA'ların işlevlerinin aydınlatılmasıy-la yeni tedavi yaklaşımları geliştirilebilecektir. Bu derlemede, miRNA'ların kardiyovasküler hastalıklarla ilişkili olduğu kuvvetli çalışmalarla ispatlanan çeşit-leri, kardiyovasküler hastalıklarla olan ilişkileri, ve tanı-tedavi amaçlı kullanımlarıyla ilgili literatüre dayalı değerlendirme yapılmıştır. Anahtar KelimelerKardiyovasküler Hastalık; Ateroskleroz; Miyokard Enfarktüsü (MI); Mikro RNA

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MicroRNA-223 coordinates cholesterol homeostasis

Cited by 226 publications

References 46 publications

Dysfunctional high-density lipoproteins in coronary heart disease: implications for diagnostics and therapy

Dysfunctional high-density lipoproteins in coronary heart disease: implications for diagnostics and therapy

miR-223 Deficiency Protects against Fas-Induced Hepatocyte Apoptosis and Liver Injury through Targeting Insulin-Like Growth Factor 1 Receptor

Unknown Aspects of Well-known Cardiovascular Diseases: Identification of Novel miRNA Genes

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