SILVA, Elsa D, Daniel PEREIRA DE SOUSA, 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 and Diana S NASCIMENTO. Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction. International Journal of Molecular Sciences. Basel: MDPI, 2024, vol. 25, No 15, p. 1-18. ISSN 1661-6596. Available from: https://dx.doi.org/10.3390/ijms25158329.
Other formats:   BibTeX LaTeX RIS
Basic information
Original name Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction
Authors SILVA, Elsa D, Daniel PEREIRA DE SOUSA (620 Portugal, belonging to the institution), 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 and Diana S NASCIMENTO.
Edition International Journal of Molecular Sciences, Basel, MDPI, 2024, 1661-6596.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30201 Cardiac and Cardiovascular systems
Country of publisher Switzerland
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 5.600 in 2022
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.3390/ijms25158329
UT WoS 001286931200001
Keywords in English myocardial infarction; pericardial fluid; fibrosis; miRNAs; miR-22-3p; cardiac fibroblasts
Tags 14110513, rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Tereza Miškechová, učo 341652. Changed: 19/8/2024 10:28.
Abstract
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.
PrintDisplayed: 21/8/2024 10:27