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@article{2421098, author = {Silva, Elsa D and Pereira de Sousa, Daniel and RibeiroandCosta, Francisco and Cerqueira, Rui and Enguita, Francisco J and Gomes, Rita N and DiasandFerreira, João and Pereira, Cassilda and Castanheira, Ana and PintoanddoandÓ, Perpétua and LeiteandMoreira, Adelino F and Nascimento, Diana S}, article_location = {Basel}, article_number = {15}, doi = {http://dx.doi.org/10.3390/ijms25158329}, keywords = {myocardial infarction; pericardial fluid; fibrosis; miRNAs; miR-22-3p; cardiac fibroblasts}, language = {eng}, issn = {1661-6596}, journal = {International Journal of Molecular Sciences}, title = {Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction}, url = {https://www.mdpi.com/1422-0067/25/15/8329}, volume = {25}, year = {2024} }
TY - JOUR ID - 2421098 AU - Silva, Elsa D - Pereira de Sousa, Daniel - Ribeiro-Costa, Francisco - Cerqueira, Rui - Enguita, Francisco J - Gomes, Rita N - Dias-Ferreira, João - Pereira, Cassilda - Castanheira, Ana - Pinto-do-Ó, Perpétua - Leite-Moreira, Adelino F - Nascimento, Diana S PY - 2024 TI - Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction JF - International Journal of Molecular Sciences VL - 25 IS - 15 SP - 1-18 EP - 1-18 PB - MDPI SN - 16616596 KW - myocardial infarction KW - pericardial fluid KW - fibrosis KW - miRNAs KW - miR-22-3p KW - cardiac fibroblasts UR - https://www.mdpi.com/1422-0067/25/15/8329 N2 - 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. ER -
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 a Diana S NASCIMENTO. Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction. \textit{International Journal of Molecular Sciences}. Basel: MDPI, 2024, roč.~25, č.~15, s.~1-18. ISSN~1661-6596. Dostupné z: https://dx.doi.org/10.3390/ijms25158329.
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