2024
Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction
SILVA, Elsa D, Daniel PEREIRA DE SOUSA, Francisco RIBEIRO-COSTA, Rui CERQUEIRA, Francisco J ENGUITA et. al.Základní údaje
Originální název
Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction
Autoři
SILVA, Elsa D, Daniel PEREIRA DE SOUSA (620 Portugalsko, domácí), Francisco RIBEIRO-COSTA, Rui CERQUEIRA, Francisco J ENGUITA, Rita N GOMES, João DIAS-FERREIRA, Cassilda PEREIRA, Ana CASTANHEIRA, Perpétua PINTO-DO-Ó, Adelino F LEITE-MOREIRA a Diana S NASCIMENTO
Vydání
International Journal of Molecular Sciences, Basel, MDPI, 2024, 1661-6596
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30201 Cardiac and Cardiovascular systems
Stát vydavatele
Švýcarsko
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 5.600 v roce 2022
Organizační jednotka
Lékařská fakulta
UT WoS
001286931200001
Klíčová slova anglicky
myocardial infarction; pericardial fluid; fibrosis; miRNAs; miR-22-3p; cardiac fibroblasts
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 19. 8. 2024 10:28, Mgr. Tereza Miškechová
Anotace
V originále
Pericardial fluid (PF) has been suggested as a reservoir of molecular targets that can be modulated for efficient repair after myocardial infarction (MI). Here, we set out to address the content of this biofluid after MI, namely in terms of microRNAs (miRs) that are important modulators of the cardiac pathological response. PF was collected during coronary artery bypass grafting (CABG) from two MI cohorts, patients with non-ST-segment elevation MI (NSTEMI) and patients with ST-segment elevation MI (STEMI), and a control group composed of patients with stable angina and without previous history of MI. The PF miR content was analyzed by small RNA sequencing, and its biological effect was assessed on human cardiac fibroblasts. PF accumulates fibrotic and inflammatory molecules in STEMI patients, namely causing the soluble suppression of tumorigenicity 2 (ST-2), which inversely correlates with the left ventricle ejection fraction. Although the PF of the three patient groups induce similar levels of fibroblast-to-myofibroblast activation in vitro, RNA sequencing revealed that PF from STEMI patients is particularly enriched not only in pro-fibrotic miRs but also anti-fibrotic miRs. Among those, miR-22-3p was herein found to inhibit TGF-beta-induced human cardiac fibroblast activation in vitro. PF constitutes an attractive source for screening diagnostic/prognostic miRs and for unveiling novel therapeutic targets in cardiac fibrosis.