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Pericardial fluid accumulates microRNAs that regulate heart fibrosis after myocardial infarction

2024-07-30Research article Open access
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dc.contributor.authorSilva, Elsa D.
dc.contributor.authorPereira-Sousa, Daniel
dc.contributor.authorRibeiro-Costa, Francisco
dc.contributor.authorCerqueira, Rui
dc.contributor.authorEnguita, Francisco J.
dc.contributor.authorGomes, Rita N.
dc.contributor.authorDias-Ferreira, João
dc.contributor.authorPereira, Cassilda
dc.contributor.authorCastanheira, Ana
dc.contributor.authorPinto-do-Ó, Perpétua
dc.contributor.authorLeite-Moreira, Adelino F.
dc.contributor.authorNascimento, Diana S.
dc.contributor.authorLopes Pereira, Cassilda Maria
dc.date.accessioned2025-05-06T08:10:42Z
dc.date.available2025-05-06T08:10:42Z
dc.date.issued2024-07-30
dc.description.abstractPericardial 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-β-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 fibrosispor
dc.description.sponsorshipPTOENSCREEN (NORTE-0145-FEDER-085468) and PPBI (PPBI-POCI-01-0145-FEDER-022122)
dc.identifier.citationSilva, E. D., Pereira-Sousa, D., Ribeiro-Costa, F., Cerqueira, R., Enguita, F. J., Gomes, R. N., Dias-Ferreira, J., Pereira, C., Castanheira, A., Pinto-do-Ó, P., Leite-Moreira, A. F., & Nascimento, D. S. (2024). Pericardial fluid accumulates microRNAs that regulate heart fibrosis after myocardial infarction. International Journal of Molecular Sciences, 25(15), Artigo 15. https://doi.org/10.3390/ijms25158329
dc.identifier.doi10.3390/ijms25158329
dc.identifier.eissn1422-0067
dc.identifier.issn1661-6596
dc.identifier.urihttp://hdl.handle.net/10400.22/30029
dc.language.isoeng
dc.peerreviewedyes
dc.publisherMDPI
dc.relation[2022.08730.PTDC; POCI-01-0145-FEDER-016385; POCI-01-0145-FEDER-030985]
dc.relation.hasversionhttps://www.mdpi.com/1422-0067/25/15/8329
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectMyocardial infarction
dc.subjectPericardial fluid
dc.subjectFibrosis
dc.subjectmiRNAs
dc.subjectmiR-22-3p
dc.subjectCardiac fibroblasts
dc.titlePericardial fluid accumulates microRNAs that regulate heart fibrosis after myocardial infarctionpor
dc.typeresearch article
dspace.entity.typePublication
oaire.citation.issue15
oaire.citation.titleInternational Journal of Molecular Sciences
oaire.citation.volume25
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
person.familyNameLopes Pereira
person.givenNameCassilda Maria
person.identifierM-4120-2013
person.identifier.ciencia-idFE17-CA18-22EC
person.identifier.orcid0000-0001-5514-4544
person.identifier.scopus-author-id44361624100
relation.isAuthorOfPublicationb91dd960-0093-4b20-8c39-c27fe3d71e8c
relation.isAuthorOfPublication.latestForDiscoveryb91dd960-0093-4b20-8c39-c27fe3d71e8c

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