Mitochondrial respiration and microRNA expression in right and left atrium of patients with atrial fibrillation.
Atrial fibrillation (AF) is the most common cardiac arrhythmia with a potential to cause serious complications. Mitochondria play central roles in cardiomyocyte function and have been implicated in AF pathophysiology. MicroRNA (miR) are suggested to influence both mitochondrial function and the development of AF. Yet mitochondrial function and miR expression remain largely unexplored in human atrial tissue. This study aims to investigate mitochondrial function and miR expression in the right (RA) and left atria (LA) of patients with AF and sinus rhythm (SR). Myocardial tissue from the RA and LA appendages was investigated in 37 patients with AF (n = 21) or SR (n = 16) undergoing coronary artery bypass surgery and/or heart valve surgery. Mitochondrial respiration was measured in situ after tissue permeabilization by saponin. MiR expression was assessed by miR array and real-time quantitative reverse-transcription polymerase chain reaction. Maximal mitochondrial respiratory rate was increased in both RA and LA tissue of patients with AF vs. SR. Biatrial downregulation of miR-208a and upregulation of miR-106b, -144, and -451 were observed in AF vs. SR. In addition, miR-15b was upregulated in AF within RA only, and miR-106a, -18a, -18b, -19a, -19b, -23a, -25, -30a, -363, -486-5p, -590-5p, and -93 were upregulated in AF within LA only. These findings suggest that mitochondrial function and miR are involved in AF pathophysiology and should be areas of focus in the exploration for potential novel therapeutic targets.
K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and technology, Trondheim, Norway; and Department of Cardiothoracic Surgery, St. Olav's University Hospital, Trondheim, Norway katrine.hordnes@ntnu.no.
Katrine Hordnes
KH
Slagsvold
K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and technology, Trondheim, Norway; and.
Anne Berit
AB
Johnsen
K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and technology, Trondheim, Norway; and.
Oivind
O
Rognmo
K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and technology, Trondheim, Norway; and.
Morten Andre
MA
Høydal
K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and technology, Trondheim, Norway; and.
Ulrik
U
Wisløff
K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and technology, Trondheim, Norway; and Department of Cardiothoracic Surgery, St. Olav's University Hospital, Trondheim, Norway.
Alexander
A
Wahba
D000368:Aged; D001281:Atrial Fibrillation / Q000235:genetics* / Q000503:physiopathology; D019069:Cell Respiration / Q000235:genetics* / Q000502:physiology; D015536:Down-Regulation / Q000235:genetics; D005260:Female; D006325:Heart Atria / Q000503:physiopathology*; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics*; D008928:Mitochondria / Q000235:genetics* / Q000502:physiology; D032383:Myocytes, Cardiac / Q000502:physiology; D015854:Up-Regulation / Q000235:genetics
D035683:MicroRNAs
atrial fibrillation; atrium; microRNA; mitochondria; myocardium