Téma: Invited guests
Číslo abstraktu: 10
Autoři: MUDr. Jana Petřková, Ph.D.; Mgr. Jana Bořucká; MUDr. Jaroslav Michálek; Prof. MUDr. Vladimír Lonský, Ph.D.; Mgr. Zdenka Navrátilová, Ph.D.; prof. MUDr. Zdeněk Kolář, CSc.; doc. MUDr. Miloš Táborský, CSc.,FESC,MBA; Prof. MUDr. Martin Petřek, CSc.
Backroung and aim: MicroRNA s (miRNA s) have been recently implicated in atherosclerosis. Underlying cause of aortic stenosis, calcific aortic valve disease (CAVD) is a process similar to atherosclerosis. We, therefore, investigated a role of 8 candidate miRNA s in patients with aortic stenosis.
Patients and methods: miR-21, -29b,- 133b, -146a, -150, -155, -181b & let-7a expression in valvular tissue from 58 aortal stenosis patients, who underwent aortic valve replacement with consent for the study, was analyzed by qRTPCR with RN U6B as reference gene. miRNA expression was compared between 2 patient subgroups: those with (n=26, A) and without (n=32, NA ) coronary atherosclerosis, defined by >30% limitation of perfusion at preoperative angiography. Valve tissues were evaluated by histopathologists to grade chronic inflammation and fibrosis extent.
Results: All investigated miRNA s were detected in all study samples. Analysis reflecting division of the study subjects into A / NA subsets showed that all studied miRNA s are upregulated in atherosclerosis, with p values ranging from 0.001 for miR-133b, to 0.01 for miR-146a, miR-181b & let-7a, to 0.02 for miR-21, miR-29b & miR-150, up to 0.03 for miR-155. Further, elevation of three miRNA s (miR-29b [p=0.04], miR-150 [0.03] and miR-181b [0.02]) was observed in patients with inflammatory infiltration of valves (n=13) compared to those without inflammation (n=24).
Conclusions: Our data support involvement of the investigated miRNA s in this valve pathology and suggest relationship of miR29b, 150 & 181b with valve inflammation. Observed upregulation of candidate miRNA s in aortal stenosis deserves further study including detailed clinical subphenotyping and characterisation of miRNA targets. Grant support: IGA PULF2013_009, CZ.1.05/2.1.00/01.0030
Datum přednesení příspěvku: 26. 4. 2013