Title
Plasma levels of microRNA in chronic kidney disease : patterns in acute and chronic exercisePlasma levels of microRNA in chronic kidney disease : patterns in acute and chronic exercise
Author
Faculty/Department
Faculty of Medicine and Health Sciences
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Research group
Translational Pathophysiological Research (TPR)
Laboratory Experimental Medicine and Pediatrics (LEMP)
Human molecular genetics
Centre for Research and Innovation in Care (CRIC)
Publication type
article
Publication
Bethesda, Md,
Subject
Human medicine
Source (journal)
American journal of physiology: heart and circulatory physiology. - Bethesda, Md
Volume/pages
309(2015):12, p. H2008-H2016
ISSN
0363-6135
ISI
000367288700003
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
Exercise training is an effective way to improve exercise capacity in chronic kidney disease (CKD) but the underlying mechanisms are only partly understood. In healthy subjects, microRNA (miR) are dynamically regulated following exercise and have therefore been suggested as regulators of cardiovascular adaptation to exercise. However, these effects were not studied in CKD before. The effect of acute exercise was assessed in 32 patients with CKD and 12 age- and sex-matched healthy subjects (HS, Study 1). MicroRNA expression in response to chronic exercise was evaluated in 40 CKD patients (Study 2). In a subgroup of Study 2, the acute-exercise induced effect was evaluated at baseline and at follow-up. Plasma levels of a panel miRNAs, involved in exercise adaptation processes such as angiogenesis (miR-126, miR-210), inflammation (miR-21, miR-146a), hypoxia/ischemia (miR-21, miR-210) and progenitor cells (miR-150), were quantified by RT PCR. Baseline, studied miR were comparable in CKD and HS. Following acute exercise, miR-150 levels increased in both CKD (fold change 2.12 ± 0.39, p=0.002 and HS: fold change 2.41 ± 0.48 p=0.018, p for interaction>0.05). miR-146a acutely decreased in CKD (fold change 0.92 ± 0.13, p=0.024), whereas it remained unchanged in HS. Levels of miR-21, miR-126 and miR-210 remained unaltered. Chronic exercise did not elicit a significant change in the studied miR levels. However, an acute exercise-induced decrease in miR-210 was observed in CKD patients, only after training. The differential expression in circulating miRNA in response to acute and chronic exercise, may point towards a physiological role in cardiovascular adaptation to exercise.
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