The function of miR-143, miR-145 and the MiR-143 host gene in cardiovascular development and disease

Vacante, Francesca; Denby, Laura; Sluimer, Judith C.; Baker, Andrew H.

doi:10.1016/j.vph.2018.11.006

Cited by 77 publications

(68 citation statements)

References 76 publications

(126 reference statements)

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“…Nonetheless, EVs contain-associated miR-143 acts as a mediator of communication between ECs and VSMCs in CVDs. miR-143 in particular is associated with vascular remodeling in pulmonary arterial hypertension (Vacante et al, 2019), while the miR-143/145 cluster, released from VSMCs, modulates angiogenesis and EC proliferation (Climent et al, 2015;Vacante et al, 2019). These findings indicate that miR-143 and miR-145 regulate VSMCs phenotype and mediate the development of vascular diseases.…”

Section: Vsmcs Contractility and Proliferationmentioning

confidence: 94%

“…Angiotensin-converting enzyme (ACE), KLF-4, myocardin Maegdefessel et al, 2013;Maegdefessel et al, 2015;Metzinger-Le Meuth et al, 2017;Ballantyne et al, 2019;Vacante et al, 2019 EVs induce numerous injury-associated responses in other vascular cells, leading to the development of CVDs (Carracedo et al, 2018a). MiRNAs are essential to the homeostasis and maintenance of EC activity (Ballantyne et al, 2019).…”

Section: Vsmcs Contractility and Proliferationmentioning

confidence: 99%

“…MiR-145 is upregulated in the plasma of patients with stable coronary artery disease, stable or unstable angina, and acute myocardial infarction (Vacante et al, 2019). Nonetheless, EVs contain-associated miR-143 acts as a mediator of communication between ECs and VSMCs in CVDs.…”

Section: Vsmcs Contractility and Proliferationmentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence

Carracedo

Alique

Vida

et al. 2020

Front. Cell Dev. Biol.

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Cardiovascular diseases (CVDs), especially those involving a systemic inflammatory process such as atherosclerosis, remain the leading cause of morbidity and mortality in patients with chronic kidney disease (CKD). CKD is a systemic condition affecting approximately 10% of the general population. The prevalence of CKD has increased over the past decades because of the aging of the population worldwide. Indeed, CVDs in patients with CKD constitute a premature form of CVD observed in the general population. Multiple studies indicate that patients with renal disease undergo accelerated aging, which precipitates the appearance of pathologies, including CVDs, usually associated with advanced age. In this review, we discuss several aspects that characterize CKD-associated CVDs, such as etiopathogenic elements that CKD patients share with the general population, changes in the cellular balance of reactive oxygen species (ROS), and the associated process of cellular senescence. Uremiaassociated aging is linked with numerous changes at the cellular and molecular level. These changes are similar to those observed in the normal process of physiologic aging. We also discuss new perspectives in the study of CKD-associated CVDs and epigenetic alterations in intercellular signaling, mediated by microRNAs and/or extracellular vesicles (EVs), which promote vascular damage and subsequent development of CVD. Understanding the processes and factors involved in accelerated senescence and other abnormal intercellular signaling will identify new therapeutic targets and lead to improved methods of diagnosis and monitoring for patients with CKD-associated CVDs.

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Section: Vsmcs Contractility and Proliferationmentioning

confidence: 94%

Section: Vsmcs Contractility and Proliferationmentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence

Carracedo

Alique

Vida

et al. 2020

Front. Cell Dev. Biol.

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“…5A, B). We selected this miRNA for further assessment because, miR-145a is predicted to target Bmp2, Smad1, 5 and 9 (Table 5, Table S3, (Vacante et al, 2019)), was also downregulated in ApoE null female mice with partial nephrectomy (Taibi et al, 2014), and improves atherosclerotic symptoms in a mouse model of hyperlipidemia (Lovren et al, miRNA replacement in aortic calcification 10 2012). The experiments described below test the impact of restoring miR-145 abundance in an alternative setting of kidney failure with accelerated aging.…”

Section: Microrna-145 and Microrna-378a Attenuation In Klotho Mutant mentioning

confidence: 99%

MicroRNA Profiles in Calcified and Healthy Aorta Differ: Therapeutic Impact of miR-145 and miR-378

Tang

Shah

Yurkow

et al. 2019

Preprint

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Our goal was to elucidate microRNAs (miRNAs) that may repress the excess bone morphogenetic protein (BMP) signaling observed during pathological calcification in the Klotho mouse model of kidney disease. We hypothesized that restoring healthy levels of miRNAs that post-transcriptionally repress osteogenic calcific factors may decrease aortic calcification. Our relative abundance profiles of miRNAs in healthy aorta differ greatly from those in calcified mouse aorta. Unbiased analyses of KEGG and GO term associated genes suggest that these miRNAs regulate proteins involved in many essential processes, including osteogenesis. Two differentially regulated miRNAs, miR-145 and miR-378, were selected based on three criteria: reduced levels in calcified aorta, the ability to target more than one protein in the BMP signaling pathway, and conservation of targeted sequences between humans and mice. Forced expression using a lentiviral vector demonstrated that restoring normal levels repressed the synthesis of BMP2 and other pro-osteogenic proteins and inhibited pathological aortic calcification in mice with renal insufficiency. This study identified miRNAs that may impact BMP signaling in both sexes and demonstrated the efficacy of selected miRNAs in reducing aortic calcification in vivo. Calcification of the aorta and the aortic valve resulting from abnormal osteogenesis is common in those with kidney disease, diabetes, and high cholesterol. Such vascular osteogenesis is a clinically significant feature. The calcification modulating miRNAs described here are candidates for biomarkers and "miRNA replacement therapies" in the context of chronic kidney disease and other pro-calcific conditions.

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“…According to the bioinformatic prediction by miRanda (http://www.microrna.org/microrna/home.do), we found a complementary sequence of microRNA-32-5p (miR-32-5p) at the 3′-untranslated region (3′-UTR) of KLF2. Numerous microRNAs (miRNAs) have been investigated in cardiovascular diseases [14,15]. The aberrant expression of miRNAs has been determined as diagnostic biomarkers or therapeutic targets in the progression of AMI [16].…”

Section: Introductionmentioning

confidence: 99%

Silence of miR-32-5p promotes endothelial cell viability by targeting KLF2 and serves as a diagnostic biomarker of acute myocardial infarction

2020

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Background: MicroRNAs (miRNAs) have been investigated in various cardiovascular diseases. As a fatal disease, acute myocardial infarction (AMI) is a serious global health burden. The purpose of this study was to investigate the role of miR-32-5p in AMI patients and human umbilical vein endothelial cells (HUVECs) to explore novel diagnostic and therapeutic approaches for AMI. Methods: A target prediction tool miRanda and the luciferase activity assay were used to confirm the interaction of miR-32-5p with Kruppel-like factor 2 (KLF2). Effect of miR-32-5p on HUVECs viability was examined using CCK-8 assay. Serum miR-32-5p expression was measured using quantitative Real-Time PCR, and its correlation with myocardial damage and endothelial injury markers and pro-inflammatory cytokines was assessed. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic value of miR-32-5p in AMI patients.Results: miR-32-5p, as a direct regulator of KLF2, could suppress the cell proliferation of HUVECs. Serum miR-32-5p expression was elevated in AMI patients and positively correlated with the biomarker levels of myocardial damage and endothelial injury and pro-inflammatory cytokines. The area under the ROC curve for miR-32-5p was 0.949, indicating the relatively high diagnostic accuracy of miR-32-5p in AMI patients. Conclusion: The data of this study revealed that the increased serum miR-32-5p expression serves as a candidate diagnostic biomarker of AMI, and that miR-32-5p may be involved in the myocardial damage, endothelial injury and inflammatory responses of AMI by targeting KLF2, indicating the potential of miR-32-5p as a diagnostic biomarker and molecular target to improve the treatment of AMI.

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The function of miR-143, miR-145 and the MiR-143 host gene in cardiovascular development and disease

Cited by 77 publications

References 76 publications

Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence

Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence

MicroRNA Profiles in Calcified and Healthy Aorta Differ: Therapeutic Impact of miR-145 and miR-378

Silence of miR-32-5p promotes endothelial cell viability by targeting KLF2 and serves as a diagnostic biomarker of acute myocardial infarction

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