دورية أكاديمية

Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction

التفاصيل البيبلوغرافية
العنوان: Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction
المؤلفون: Elsa D. Silva, Daniel Pereira-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, Diana S. Nascimento
المصدر: International Journal of Molecular Sciences, Vol 25, Iss 15, p 8329 (2024)
بيانات النشر: MDPI AG, 2024.
سنة النشر: 2024
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: myocardial infarction, pericardial fluid, fibrosis, miRNAs, miR-22-3p, cardiac fibroblasts, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: 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-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 fibrosis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
1661-6596
Relation: https://www.mdpi.com/1422-0067/25/15/8329; https://doaj.org/toc/1661-6596; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms25158329
URL الوصول: https://doaj.org/article/d628a55862eb4a6cbab616ba720120f3
رقم الأكسشن: edsdoj.628a55862eb4a6cbab616ba720120f3
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
16616596
DOI:10.3390/ijms25158329