Abstract
Aim: mircoRNAs (miRNAs), small non-coding RNAs regulating gene expression, are stably secreted into the blood and circulating miRNAs (c-miRNAs) may play an important role in cell–cell communication. Furthermore, c-miRNAs might serve as novel biomarkers of the current vascular cell status. Here, we examined how the levels of three vascular c-miRNAs (c-miR-16, c-miR-21, c-miR-126) are acutely affected by different exercise intensities and volumes.Methods: 12 subjects performed 3 different endurance exercise protocols: 1. High-Volume Training (HVT; 130 min at 55% peak power output (PPO); 2. High-Intensity Training (HIT; 4 × 4 min at 95% PPO); 3. Sprint-Interval Training (SIT; 4 × 30 s all-out). c-miRNAs were quantified using quantitative real-time PCR with TaqMan probes at time points pre, 0′, 30′, 60′, and 180′ after each intervention. The expression of miR-126 and miR-21 was analyzed in vitro, in human coronary artery endothelial cells, human THP-1 monocytes, human platelets, human endothelial microparticles (EMPs) and human vascular smooth muscle cells (VSMCs). To investigate the transfer of miRNAs via EMPs, VSMCs were incubated with EMPs.Results: HVT and SIT revealed large increases on c-miR-21 [1.9-fold by HVT (cohen's d = 0.85); 1.5-fold by SIT (cohen's d = 0.85)] and c-miR-126 [2.2-fold by SIT (cohen's d = 1.06); 1.9-fold by HVT (cohen's d = 0.85)] post-exercise compared to pre-values, while HIT revealed only small to moderate changes on c-miRs-21 (cohen's d = −0.28) and c-miR-126 (cohen's d = 0.53). c-miR-16 was only slightly affected by SIT (1.4-fold; cohen's d = 0.57), HVT (1.3-fold; cohen's d = 0.61) or HIT (1.1-fold; cohen's d = 0.2). Further in vitro experiments revealed that miR-126 and miR-21 are mainly of endothelial origin. Importantly, under conditions of endothelial apoptosis, miR-126 and miR-21 are packed from endothelial cells into endothelial microparticles, which were shown to transfer miR-126 into target vascular smooth muscle cells.Conclusion: Taken together, we found that HVT and SIT are associated with the release of endothelial miRNAs into the circulation, which can function as intercellular communication devices regulating vascular biology.
Highlights
Endurance training is known to have positive effects on endothelial function and to induce angiogenesis [defined as the formation of new blood vessels from pre-existing vessels, in particular, capillaries (Brown and Hudlicka, 2003)]
We have shown that endurance exercise, independent of intensity, led to decreased endothelial microparticle (EMP) levels and promoted a phosphatidylserine-dependent uptake of EMP into target endothelial cells, which was associated with a protection of target cells against apoptosis (Wahl et al, 2014)
The changes in PV ranged from −6.2% to +8.5% 0′ and 180′ after Sprint-Interval Training (SIT), −5.2% to +3.5% 0′ and 180′after HighIntensity Training (HIT) and, −0.9% to +5.6% 0′ and 180′ after High-Volume Training (HVT), respectively
Summary
Endurance training is known to have positive effects on endothelial function and to induce angiogenesis [defined as the formation of new blood vessels from pre-existing vessels, in particular, capillaries (Brown and Hudlicka, 2003)]. MicroRNAs (miRNAs) are small non-coding RNAs of 18–22 nucleotides in length, which post-transcriptionally regulate gene expression via mRNA degradation or translational inhibition (Xu et al, 2015). MiRNAs can be released into the circulation where they exist in stable forms and play important roles in a wide range of physiological and pathological processes (Ambros, 2004; Mooren et al, 2014). C-miRNAs have been suggested as new and alternative biomarkers of muscle damage (Banzet et al, 2013), myocardial infarction (Da Costa Martins and De Windt, 2012), cardiovascular health (Bye et al, 2013), or aerobic performance (Mooren et al, 2014). Expression changes of miRNAs may reflect responses to exercise more in detail compared to conventional plasmabased markers, such as creatine-kinase, lactate-dehydrogenase, troponin, C-reactive protein, or interleukin-6 (Baggish et al, 2014; Mooren et al, 2014)
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