Acute Effects of Different Exercise Protocols on the Circulating Vascular microRNAs -16, -21, and -126 in Trained Subjects

Wahl, Patrick; Wehmeier, Udo F.; Jansen, Felix; Kilian, Yvonne; Bloch, Wilhelm; Werner, Nikos; Mester, Joachim; Hilberg, Thomas

doi:10.3389/fphys.2016.00643

Cited by 52 publications

(44 citation statements)

References 50 publications

(79 reference statements)

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“…Their results suggest that exercise can also improve miR-126 levels in the circulation. In vitro findings have suggested that miR-126 is mainly of endothelial origin [38]. In addition, Wang et al [39] found that miR-126 overexpression significantly increased EPC colony formation, proliferation, and migration and reduc apoptosis in patients with diabetic vascular disease when compared to the control.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Screened microRNAs related to endothelial progenitor cells and verified the target gene of microRNA-126-3p

Deng¹,

Xu²,

Li³

et al. 2018

Oncotarget

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Background: Endothelial progenitor cell play a vital role in neovascularization. Exercise-based cardiac rehabilitation significantly increases endothelial progenitor cells number and functions in patients with ischemic disease. Exercise can also increase the level of endothelial microRNAs. We hypothesized that microRNAs participate in regulating endothelial progenitor cell function under aerobic exercise. Thus, we attempted to identify such microRNAs and to verify the miR-126-3p target gene.Methods: Microarray is used to screen the microRNAs. The prediction programs TargetScan is used to predict the miR-126-3p target gene. Experimental EPCs are treated with miR-126-3p mimics. The relative expression of miR-126-3p and Mus musculus sprouty-related EVH1 domain-containing 1 (Spred1) are examined using real-time PCR and western blot. The dual-luciferase reporter assay is used to verify the miR-126-3p target gene.Results: The miR-126-3p target genes included those contributing to angiogenesis and revascularization. The predicted miR-126-3p target gene is Spred1. Compared with the control, miR-126-3p relative expression is highest following 48-h treatment with 50 nM miR-126-3 mimic. Spred1 mRNA and protein expression in the experimental group is 40.7% and 45.7%. The ratio of Renilla and firefly luciferase activity in the wild-type group is 88.3% and 74.2% of the control respectively (all, n = 3, p < 0.001).Conclusion: miR-126-3p participates in regulating endothelial progenitor cell function after aerobic exercise. MiR-126-3p inhibits the transcription and translation of Spred1, the target gene of miR-126-3p.

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Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Screened microRNAs related to endothelial progenitor cells and verified the target gene of microRNA-126-3p

Deng¹,

Xu²,

Li³

et al. 2018

Oncotarget

View full text Add to dashboard Cite

show abstract

“…Of these genes, there is much evidence that SPRED1 is a target of miR‐126 in promoting angiogenesis . Interestingly, recent studies have not only revealed important roles for miR‐126 in response to cardiac ischaemia, but have also demonstrated that exercise up‐regulates miR‐126 expression . Accordingly, we speculated that miR‐126 may up‐regulate exercise‐induced EPC function in mice after MI.…”

Section: Introductionmentioning

confidence: 99%

TPPU enhanced exercise‐induced epoxyeicosatrienoic acid concentrations to exert cardioprotection in mice after myocardial infarction

Guo

Luo

Zhang

et al. 2017

J Cellular Molecular Medi

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Exercise training (ET) is a safe and efficacious therapeutic approach for myocardial infarction (MI). Given the numerous benefits of exercise, exercise‐induced mediators may be promising treatment targets for MI. C57BL/6 mice were fed 1‐trifluoromethoxyphenyl‐3‐(1‐propionylpiperidine‐4‐yl) urea (TPPU), a novel soluble epoxide hydrolase inhibitor (sEHI), to increase epoxyeicosatrienoic acid (EET) levels, for 1 week before undergoing MI surgery. After 1‐week recovery, the mice followed a prescribed exercise programme. Bone marrow‐derived endothelial progenitor cells (EPCs) were isolated from the mice after 4 weeks of exercise and cultured for 7 days. Angiogenesis around the ischaemic area, EPC functions, and the expression of microRNA‐126 (miR‐126) and its target gene Spred1 were measured. The results were confirmed in vitro by adding TPPU to EPC culture medium. ET significantly increased serum EET levels and promoted angiogenesis after MI. TPPU enhanced the effects of ET to reduce the infarct area and improve cardiac function after MI. ET increased EPC function and miR‐126 expression, which were further enhanced by TPPU, while Spred1 expression was significantly down‐regulated. Additionally, the protein kinase B/glycogen synthase kinase 3β (AKT/GSK3β) signalling pathway was activated after the administration of TPPU. EETs are a potential mediator of exercise‐induced cardioprotection in mice after MI. TPPU enhances exercise‐induced cardiac recovery in mice after MI by increasing EET levels and promoting angiogenesis around the ischaemic area.

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“…; Wahl et al. ) and longer exercise training interventions (Taurino et al. ; Van Craenenbroeck et al.…”

Section: Discussionmentioning

confidence: 99%

Small non-coding RNAs are altered by short-term sprint interval training in men

et al. 2018

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Small non‐coding RNAs (ncRNAs) are emerging as important molecules for normal biological processes and are deregulated in disease. Exercise training is a powerful therapeutic strategy that prevents cardiometabolic disease and improves cardiorespiratory fitness and performance. Despite the known systemic health benefits of exercise training, the underlying molecular mechanisms are incompletely understood. Recent evidence suggests a role for epigenetic mechanisms, such as microRNAs, but whether other small ncRNAs are modulated by chronic exercise training is unknown. Here, we used small RNA sequencing to explore whether sprint interval training (SIT) controls the abundance of circulating small ncRNAs in human whole blood samples. Ten healthy men performed SIT three times a week for 6 weeks. After training, subjects showed marked improvements in maximal oxygen consumption and cycling performance with concurrent changes to the abundance of diverse species of circulating small ncRNAs (n = 1266 small ncRNAs, n = 13 microRNAs, q < 0.05). Twelve microRNAs altered by 6 weeks of SIT were ubiquitously expressed microRNAs and two regulated important signaling pathways, including p53, thyroid hormone and cell cycle signaling. MicroRNAs altered by 6 weeks of SIT were unchanged after a single session of SIT (n = 24, all P > 0.05). Relative to older individuals, younger subjects exhibited an increased acute SIT‐induced fold change in miR‐1301‐3p (P = 0.02) – a microRNA predicted to target mRNAs involved in alternative splicing, phosphoprotein and chromosomal rearrangement processes (all P < 0.001). Our findings indicate many species of circulating small ncRNAs are modulated by exercise training and that they could control signaling pathways responsible for health benefits achieved from exercise.

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Acute Effects of Different Exercise Protocols on the Circulating Vascular microRNAs -16, -21, and -126 in Trained Subjects

Cited by 52 publications

References 50 publications

WITHDRAWN: Screened microRNAs related to endothelial progenitor cells and verified the target gene of microRNA-126-3p

WITHDRAWN: Screened microRNAs related to endothelial progenitor cells and verified the target gene of microRNA-126-3p

TPPU enhanced exercise‐induced epoxyeicosatrienoic acid concentrations to exert cardioprotection in mice after myocardial infarction

Small non-coding RNAs are altered by short-term sprint interval training in men

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