MicroRNA-150 Protects the Heart From Injury by Inhibiting Monocyte Accumulation in a Mouse Model of Acute Myocardial Infarction

Liu, Zheng; Ye, Ping; Wang, Sihua; Wu, Jie; Sun, Yuan; Zhang, Anchen; Ren, Linyun; Cheng, Chao; Huang, Xintang; Wang, Ke; Deng, Peng; Wu, Chuangyan; Zhang, Yue; Xia, Jiahong

doi:10.1161/circgenetics.114.000598

Cited by 65 publications

(66 citation statements)

References 35 publications

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“…In a previous study, we found that plasma miR-150 levels were significantly associated with atrial fibrillation severity [23]. We also demonstrated that miR-150 disturbs the inflammatory response of peripheral blood monocytes in myocardial infarction by targeting CXCR4 [24]. These results suggest that miR-150 in peripheral blood can regulate the occurrence and development of cardiovascular diseases, such as myocardial infarction.…”

Section: Discussionmentioning

confidence: 66%

“…In our previous studies, we found that plasma miR-150 level was positively associated with atrial fibrillation severity [23]. We also observed that miR-150 regulates the migration of monocytes to the area of myocardial infarction by targeting CXCR4, thereby reducing the occurrence and development of myocardial fibrosis and protecting heart function [24]. These results suggest that miR-150 in peripheral blood can regulate the occurrence and development of cardiac fibrosis.…”

Section: Introductionmentioning

confidence: 73%

“…Mouse cardiac function was measured using a Vevo 2100 high-resolution micro-imaging system with a 30-MHz transducer (VisualSonics, Toronto, Ontario, Canada), as described previously [24]. In brief, the mice were anesthetized with 0.5% pentobarbital sodium (75 mg/kg, i.p.).…”

Section: Methodsmentioning

confidence: 99%

“…Then, the mid-ventricular short axis and parasternal long axis were imaged using M-model echocardiography. The left ventricular ejection fraction (EF) and fractional shortening (FS) were assessed from the digital images, using the root of the ventricular papillary muscle as the baseline as well as the methods described previously [24]. Echocardiographic acquisition and analysis were performed by a technician who was blinded to the treatment groups.…”

Section: Methodsmentioning

confidence: 99%

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MicroRNA-150 Inhibits the Activation of Cardiac Fibroblasts by Regulating c-Myb

Deng

Chen

Liu

et al. 2016

Cell Physiol Biochem

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Background/Aims: Cardiac fibrosis is the primary cause of deteriorated cardiac function in various cardiovascular diseases. Numerous studies have demonstrated that microRNAs (miRNAs) are critical regulators of myocardial fibrosis. Specifically, many studies have reported that miR-150 is downregulated in cardiovascular diseases, such as acute myocardial infarction (AMI), myocardial hypertrophy and myocardial fibrosis. However, the exact role of miR-150 in these pathological processes remains unknown. Methods: We used the transverse aortic constriction (TAC) mouse model to study the role of miR-150 in cardiac fibrosis induced by pressure overload. After the TAC operation, qRT-PCR was used to measure the expression profiles of miR-150 in left ventricle tissues and populations of primary heart cell types. Then, we used both miR-150 knockout mice and wild type (WT) mice in the TAC model. Changes in cardiac function and pathology were measured using transthoracic echocardiography and pathological analysis, respectively. Furthermore, we predicted the target of miR-150 in cardiac fibroblasts (CFs) and completed in vitro CF transfection experiments using miR-150 analogs and siRNA corresponding to the predicted target. Results: We observed decreased expression levels of miR-150 in hearts suffering pressure overload, and these levels decreased more sharply in CFs than in cardiomyocytes. In addition, the degrees of cardiac function deterioration and cardiac fibrosis in miR-150-/- mice were more severe than were those in WT mice. By transfecting CFs with an miR-150 analog in vitro, we observed that miR-150 inhibited cardiac fibroblast activation. We predicted that the transcription factor c-Myb was the target of miR-150 in CFs. Transfecting CFs with c-Myb siRNA eliminated the effects of an miR-150 inhibitor, which promoted CF activation. Conclusion: These findings reveal that miR-150 acts as a pivotal regulator of pressure overload-induced cardiac fibrosis by regulating c-Myb.

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Section: Discussionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 73%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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MicroRNA-150 Inhibits the Activation of Cardiac Fibroblasts by Regulating c-Myb

Deng

Chen

Liu

et al. 2016

Cell Physiol Biochem

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“…Specifically, miR-150 is predicted to target the inflammatory mediator IL-18 and is down-regulated in sepsis patients and following exposure of cells to bacterial lipopolysaccharide (LPS) in vitro (32, 33). Furthermore, Liu et al demonstrated miR-150 overexpression reduces inflammatory mediators (TNF-α, IL-1β, and IL-6) in monocytes (34). …”

Section: Introductionmentioning

confidence: 99%

Dysregulation of microRNA biogenesis in the small intestine after ethanol and burn injury

Morris

Hammer

Cannon

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Ethanol exposure at the time of burn injury is a major contributor to post-burn pathogenesis. Many of the adverse effects associated with ethanol and burn injury are linked to an impaired intestinal barrier. The combined insult causes intestinal inflammation, resulting in tissue damage, altered tight junction expression, and increased intestinal permeability. microRNAs play a critical role in maintaining intestinal homeostasis including intestinal inflammation and barrier function. Specifically, miR-150 regulates inflammatory mediators which can contribute to gut barrier disruption. The present study examined whether ethanol and burn injury alters expression of microRNA processing enzymes (Drosha, Dicer, and Argonaute-2) and miR-150 in the small intestine. Male mice were gavaged with ethanol (~2.9g/kg) 4 hours prior to receiving a ~12.5% total body surface area full thickness burn. One or three days after injury, mice were euthanized and small intestinal epithelial cells (IECs) were isolated and analyzed for expression of microRNA biogenesis components and miR-150. Dicer mRNA and protein levels were not changed following the combined insult. Drosha and Argonaute-2 mRNA and protein levels were significantly reduced in IECs one day after injury; which accompanied reduced miR-150 expression. To further determine the role of miR-150 in intestinal inflammation, young adult mouse colonocytes were transfected with a miR-150 plasmid and stimulated with LPS (100ng/mL). miR-150 overexpression significantly reduced IL-6 and KC protein levels compared to vector control cells challenged with LPS. These results suggest that altered microRNA biogenesis and associated decrease in miR-150 likely contributes to increased intestinal inflammation following ethanol and burn injury.

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Knockdown of Long Non‐Coding RNA‐ZFAS1 Protects Cardiomyocytes Against Acute Myocardial Infarction Via Anti‐Apoptosis by Regulating miR‐150/CRP

et al. 2017

J of Cellular Biochemistry

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ZFAS1 is one of cardiac-specific or cardiac-related lncRNAs. This study was to explore the functional involvement of ZFAS1 and its regulatory role in AMI. In this study, the models of AMI rat and myocardial cell cultured under hypoxia were made. The expression of ZFAS1 and miR-150 of myocardial infarction tissue or cardiac myocytes was determined by quantitative real time PCR. The regulatory role of ZFAS1 on miR-150 was examined by RNA pull down assay. The effect of miR-150 or ZFAS1 expression on cell viability was analyzed by MTT assay. The relative expression of ZFAS1 in the myocardium infracted zone and border zone was significantly upregulated at 1-48 h of AMI rats, but it downregulated at 1 week and 2 weeks; miR-150 was significantly downregulated at AMI-1-48 h and upregulated at 1 and 2 weeks after model establishment. The result of RNA pull down assay indicated that ZFAS1 could interact directly with miR-150. C-reactive protein (CRP) was regulated by ZFAS1/miR-150 axis and negatively targeted by miR-150. Hypoxia caused the decrease of cell viability and the upregulation of CRP at mRNA and protein levels; whereas this upregulation could be attenuated by miR-150 mimic or si-ZFAS1 in H9C2 cells and cardiomyocytes. Knockdown of ZFAS1 or miR-150 overexpression effectively relieved AMI-induced myocardial infarction in AMI-1 week rats. The ZFAS1/miR-150 axis was involved in the molecular mechanism of AMI induced cardiomyocytes apoptosis via regulating CRP. J. Cell. Biochem. 118: 3281-3289, 2017. © 2017 Wiley Periodicals, Inc.

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MicroRNA-150 Protects the Heart From Injury by Inhibiting Monocyte Accumulation in a Mouse Model of Acute Myocardial Infarction

Cited by 65 publications

References 35 publications

MicroRNA-150 Inhibits the Activation of Cardiac Fibroblasts by Regulating c-Myb

MicroRNA-150 Inhibits the Activation of Cardiac Fibroblasts by Regulating c-Myb

Dysregulation of microRNA biogenesis in the small intestine after ethanol and burn injury

Knockdown of Long Non‐Coding RNA‐ZFAS1 Protects Cardiomyocytes Against Acute Myocardial Infarction Via Anti‐Apoptosis by Regulating miR‐150/CRP

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