Circulating microRNA changes in patients with impaired glucose regulation

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ABSTRACT

We analysed if levels of four miRNAs would change after a lifestyle intervention involving dietary and exercises in prediabetes. MiRNAs previously shown to be associated with diabetes (Let-7a, Let-7e, miR-144 and miR-92a) were extracted from serum pre- and post-intervention. mRNA was extracted from fat-tissue for gene expression analyses. The intervention resulted in increased Let-7a and miR-92a. We found correlations between miRNAs and clinical variables (triglycerides, cholesterol, insulin, weight and BMI). We also found correlations between miRNAs and target genes, revealing a link between miR-92a and IGF system. A lifestyle intervention resulted in marked changes in miRNAs. The association of miRNAs with insulin and the IGF system (both receptors and binding proteins) may represent a mechanism of regulating IGFs metabolic actions.

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MicroRNA-92a controls angiogenesis and functional recovery of ischemic tissues in mice.

Angelika Bonauer, Guillaume Carmona, Masayoshi Iwasaki … (2009)

MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression by binding to target messenger RNAs (mRNAs), leading to translational repression or degradation. Here, we show that the miR-17approximately92 cluster is highly expressed in human endothelial cells and that miR-92a, a component of this cluster, controls the growth of new blood vessels (angiogenesis). Forced overexpression of miR-92a in endothelial cells blocked angiogenesis in vitro and in vivo. In mouse models of limb ischemia and myocardial infarction, systemic administration of an antagomir designed to inhibit miR-92a led to enhanced blood vessel growth and functional recovery of damaged tissue. MiR-92a appears to target mRNAs corresponding to several proangiogenic proteins, including the integrin subunit alpha5. Thus, miR-92a may serve as a valuable therapeutic target in the setting of ischemic disease.

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Inhibition of microRNA-92a prevents endothelial dysfunction and atherosclerosis in mice.

Pierre Julia, Anne Vion, Jean-Claude Paul … (2014)

MicroRNAs (miRNAs) are small noncoding RNAs that regulate protein expression at post-transcriptional level. We hypothesized that a specific pool of endothelial miRNAs could be selectively regulated by flow conditions and inflammatory signals, and as such be involved in the development of atherosclerosis. To identify miRNAs, called atheromiRs, which are selectively regulated by shear stress and oxidized low-density lipoproteins (oxLDL), and to determine their role in atherogenesis. Large-scale miRNA profiling in HUVECs identified miR-92a as an atheromiR candidate, whose expression is preferentially upregulated by the combination of low shear stress (SS) and atherogenic oxLDL. Ex vivo analysis of atheroprone and atheroprotected areas of mouse arteries and human atherosclerotic plaques demonstrated the preferential expression of miR-92a in atheroprone low SS regions. In Ldlr(-/-) mice, miR-92a expression was markedly enhanced by hypercholesterolemia, in particular in atheroprone areas of the aorta. Assessment of endothelial inflammation in gain- and loss-of-function experiments targeting miR-92a expression revealed that miR-92a regulated endothelial cell activation by oxLDL, more specifically under low SS conditions, which was associated with modulation of Kruppel-like factor 2 (KLF2), Kruppel-like factor 4 (KLF4), and suppressor of cytokine signaling 5. miR-92a expression was regulated by signal transducer and activator of transcription 3 in SS- and oxLDL-dependent manner. Furthermore, specific in vivo blockade of miR-92a expression in Ldlr(-/-) mice reduced endothelial inflammation and altered the development of atherosclerosis, decreasing plaque size and promoting a more stable lesion phenotype. Upregulation of miR-92a by oxLDL in atheroprone areas promotes endothelial activation and the development of atherosclerotic lesions. Therefore, miR-92a antagomir seems as a new atheroprotective therapeutic strategy.

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Type 2 Diabetes Mellitus and Cardiovascular Disease: Genetic and Epigenetic Links

Salvatore De Rosa, Biagio Arcidiacono, Eusebio Chiefari … (2018)

Type 2 diabetes mellitus (DM) is a common metabolic disorder predisposing to diabetic cardiomyopathy and atherosclerotic cardiovascular disease (CVD), which could lead to heart failure through a variety of mechanisms, including myocardial infarction and chronic pressure overload. Pathogenetic mechanisms, mainly linked to hyperglycemia and chronic sustained hyperinsulinemia, include changes in metabolic profiles, intracellular signaling pathways, energy production, redox status, increased susceptibility to ischemia, and extracellular matrix remodeling. The close relationship between type 2 DM and CVD has led to the common soil hypothesis, postulating that both conditions share common genetic and environmental factors influencing this association. However, although the common risk factors of both CVD and type 2 DM, such as obesity, insulin resistance, dyslipidemia, inflammation, and thrombophilia, can be identified in the majority of affected patients, less is known about how these factors influence both conditions, so that efforts are still needed for a more comprehensive understanding of this relationship. The genetic, epigenetic, and environmental backgrounds of both type 2 DM and CVD have been more recently studied and updated. However, the underlying pathogenetic mechanisms have seldom been investigated within the broader shared background, but rather studied in the specific context of type 2 DM or CVD, separately. As the precise pathophysiological links between type 2 DM and CVD are not entirely understood and many aspects still require elucidation, an integrated description of the genetic, epigenetic, and environmental influences involved in the concomitant development of both diseases is of paramount importance to shed new light on the interlinks between type 2 DM and CVD. This review addresses the current knowledge of overlapping genetic and epigenetic aspects in type 2 DM and CVD, including microRNAs and long non-coding RNAs, whose abnormal regulation has been implicated in both disease conditions, either etiologically or as cause for their progression. Understanding the links between these disorders may help to drive future research toward an integrated pathophysiological approach and to provide future directions in the field.

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Author and article information

Journal

Journal ID (nlm-ta): Adipocyte

Journal ID (iso-abbrev): Adipocyte

Title: Adipocyte

Publisher: Taylor & Francis

ISSN (Print): 2162-3945

ISSN (Electronic): 2162-397X

Publication date (Electronic, pub): 4 August 2020

Publication date (Electronic, collection): 2020

Publication date PMC-release: 4 August 2020

Volume: 9

Issue: 1

Pages: 443-453

Affiliations

[a ]The School of Medicine and Manchester Academic Health Sciences Centre, University of Manchester;

[b ]Department of Diabetes and Endocrinology, Salford Royal Hospital; , Salford, UK

[c ]Biomolecular Sciences Research Centre, Sheffield Hallam University; , Sheffield, UK

[d ]Department of Diabetes Complications and Metabolism, Beckman Research Institute, City of Hope; , Duarte, CA, USA

Author notes

CONTACT Adrian H. Heald adrian.heald@ 123456manchester.ac.uk Department of Diabetes and Endocrinology, Salford Royal Hospital; , SalfordM6 8HD, UK

Author information

Helene A. Fachim https://orcid.org/0000-0003-3818-3167

Camila M. Loureiro https://orcid.org/0000-0002-0239-5064

Kirk Siddals https://orcid.org/0000-0002-4647-3140

Caroline F Dalton https://orcid.org/0000-0002-1404-873X

Gavin P. Reynolds https://orcid.org/0000-0001-9026-7726

J. Martin Gibson https://orcid.org/0000-0002-1331-1524

Zhen Bouman Chen https://orcid.org/0000-0002-3291-1090

Adrian H. Heald https://orcid.org/0000-0002-9537-4050

Article

Publisher ID: 1798632

DOI: 10.1080/21623945.2020.1798632

PMC ID: 7469475

PubMed ID: 32752917

SO-VID: 58db0666-f91d-4adc-ade1-796ec10d04cc

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Circulating microRNA changes in patients with impaired glucose regulation

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Most cited references 35

MicroRNA-92a controls angiogenesis and functional recovery of ischemic tissues in mice.

Inhibition of microRNA-92a prevents endothelial dysfunction and atherosclerosis in mice.

Type 2 Diabetes Mellitus and Cardiovascular Disease: Genetic and Epigenetic Links

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