Mehmet Bulent Vatan1, Aysel Kalaycı Yigin2, Ramazan Akdemir3, Mustafa Tarik Agac3, Mehmet Akif Cakar3, Murat Aksoy3, Ersan Tatli3, Harun Kilic3, Huseyin Gunduz3, Derya Guzel4, Keziban Karacan5. 1. Department of Cardiology, Sakarya University School of Medicine, Sakarya, Turkey. Electronic correspondence: bulentvatan@hotmail.com. 2. Department of Medical Biology and Genetics, Sakarya University School of Medicine, Sakarya, Turkey. 3. Department of Cardiology, Sakarya University School of Medicine, Sakarya, Turkey. 4. Department of Physiology, Sakarya University School of Medicine, Sakarya, Turkey. 5. Department of Anatomy, Sakarya University School of Medicine, Sakarya, Turkey.
Abstract
BACKGROUND: Mitral chordae tendineae rupture (MCTR) is a progressive disorder which leads to severe mitral regurgitation. Despite its importance, the precise pathogenetic mechanism of MCTR remains unclear. The study aim was to investigate the expression profile of circulating microRNAs (miRNAs) as being potentially involved in the development of MCTR. METHODS: Twenty-one patients with 'primary' MCTR, and 30 age- and gender-matched controls, were enrolled in the study. Comparisons were made between the expression levels of circulating miRNAs in MCTR patients and controls. Four target gene databases were used to predict target genes and pathways of differentially expressed miRNAs. RESULTS: Compared to controls, the expression of 22 miRNAs (hsa-miR-106b-5p, hsa-miR-126-3p, hsa-miR-150-5p, hsa-miR-17-5p, hsa-miR-195-5p, hsa-miR-19a-3p, hsa-miR-19b-3p, hsa-miR-20a-5p, hsa-miR-21-5p, hsa-miR-222-3p, hsa-miR-223-3p, hsa-miR-23a-3p, hsa-miR-25-3p, hsa-miR-92a-3p, hsa-miR-93-5p, hsa-miR-26b-5p, hsa-miR-30e-5p, hsa-miR-373-3p, hsa-miR-15b-5p, hsa-miR-16-5p, hsa-miR-191-5p, hsa-miR-26a-5p) were significantly down-regulated in the MCTR group. Bioinformatic analysis indicated that the following potential miRNA targets and pathways are commonly related to the development of MCTR: MMPs, TIMP-2,TGFBR2, VEGFA, PIK3R2, NRAS, PPP3CA, PPP3R1, PTGS 2 were predicted as putative targets of 13 of these miRNAs. CONCLUSIONS: The present study is the first to describe altered miRNA expression in patients with MCTR. Bioinformatic analysis has revealed that target genes involved in MCTR development were regulated by miRNAs.
BACKGROUND:Mitral chordae tendineae rupture (MCTR) is a progressive disorder which leads to severe mitral regurgitation. Despite its importance, the precise pathogenetic mechanism of MCTR remains unclear. The study aim was to investigate the expression profile of circulating microRNAs (miRNAs) as being potentially involved in the development of MCTR. METHODS: Twenty-one patients with 'primary' MCTR, and 30 age- and gender-matched controls, were enrolled in the study. Comparisons were made between the expression levels of circulating miRNAs in MCTR patients and controls. Four target gene databases were used to predict target genes and pathways of differentially expressed miRNAs. RESULTS: Compared to controls, the expression of 22 miRNAs (hsa-miR-106b-5p, hsa-miR-126-3p, hsa-miR-150-5p, hsa-miR-17-5p, hsa-miR-195-5p, hsa-miR-19a-3p, hsa-miR-19b-3p, hsa-miR-20a-5p, hsa-miR-21-5p, hsa-miR-222-3p, hsa-miR-223-3p, hsa-miR-23a-3p, hsa-miR-25-3p, hsa-miR-92a-3p, hsa-miR-93-5p, hsa-miR-26b-5p, hsa-miR-30e-5p, hsa-miR-373-3p, hsa-miR-15b-5p, hsa-miR-16-5p, hsa-miR-191-5p, hsa-miR-26a-5p) were significantly down-regulated in the MCTR group. Bioinformatic analysis indicated that the following potential miRNA targets and pathways are commonly related to the development of MCTR: MMPs, TIMP-2,TGFBR2, VEGFA, PIK3R2, NRAS, PPP3CA, PPP3R1, PTGS 2 were predicted as putative targets of 13 of these miRNAs. CONCLUSIONS: The present study is the first to describe altered miRNA expression in patients with MCTR. Bioinformatic analysis has revealed that target genes involved in MCTR development were regulated by miRNAs.
Authors: Abel Decmann; Gábor Nyírö; Ottó Darvasi; Péter Turai; Irina Bancos; Ravinder Jeet Kaur; Raffaele Pezzani; Maurizio Iacobone; Ivana Kraljevic; Darko Kastelan; Mirko Parasiliti-Caprino; Mauro Maccario; Nina Nirschl; Daniel Heinrich; Martin Reincke; Attila Patócs; Peter Igaz Journal: Front Endocrinol (Lausanne) Date: 2019-10-29 Impact factor: 5.555