J 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

Štítky

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.