dc.contributor.author |
Bellera Gotarda, Neus |
dc.contributor.author |
Barba, Ignasi |
dc.contributor.author |
Rodriguez-Sinovas, Antonio |
dc.contributor.author |
Ferret, Eulalia |
dc.contributor.author |
Asín, Miguel Angel |
dc.contributor.author |
Gonzalez-Alujas, MªTeresa |
dc.contributor.author |
Pérez-Rodón, Jordi |
dc.contributor.author |
Esteves, Marielle |
dc.contributor.author |
Fonseca, Carla |
dc.contributor.author |
Toran, Nuria |
dc.contributor.author |
García del Blanco, Bruno |
dc.contributor.author |
Pérez, Amadeo |
dc.contributor.author |
García-Dorado, David |
dc.contributor.author |
Universitat Autònoma de Barcelona |
dc.date |
2014 |
dc.identifier |
https://ddd.uab.cat/record/185098 |
dc.identifier |
urn:10.1161/JAHA.114.000946 |
dc.identifier |
urn:oai:ddd.uab.cat:185098 |
dc.identifier |
urn:pmid:25240056 |
dc.identifier |
urn:pmcid:PMC4323815 |
dc.identifier |
urn:pmc-uid:4323815 |
dc.identifier |
urn:scopus_id:84923551127 |
dc.identifier |
urn:wos_id:000341861200004 |
dc.identifier |
urn:altmetric_id:2709357 |
dc.identifier |
urn:oai:egreta.uab.cat:publications/ce2dce09-0229-485a-85dd-d8c82c6bbae5 |
dc.identifier |
urn:oai:pubmedcentral.nih.gov:4323815 |
dc.format |
application/pdf |
dc.language |
eng |
dc.publisher |
|
dc.relation |
Ministerio de Ciencia e Innovación SAF 2008-03067 |
dc.relation |
Instituto de Salud Carlos III RD12-0042-0021 |
dc.relation |
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease ; Vol. 3 (september 2014) |
dc.rights |
open access |
dc.rights |
Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original. |
dc.rights |
https://creativecommons.org/licenses/by-nc/4.0/ |
dc.subject |
Angiogenesis |
dc.subject |
Antagomir |
dc.subject |
Heart failure |
dc.subject |
MicroRNA |
dc.subject |
Myocardial infarction |
dc.subject |
Remodeling |
dc.title |
Single Intracoronary Injection of Encapsulated Antagomir-92a Promotes Angiogenesis and Prevents Adverse Infarct Remodeling |
dc.type |
Article |
dc.description.abstract |
Small and large preclinical animal models have shown that antagomir-92a-based therapy reduces early postischemic loss of function, but its effect on postinfarction remodeling is not known. In addition, the reported remote miR-92a inhibition in noncardiac organs prevents the translation of nonvectorized miR-targeted therapy to the clinical setting. We investigated whether a single intracoronary administration of antagomir-92a encapsulated in microspheres could prevent deleterious remodeling of myocardium 1 month after acute myocardial infarction AUTHOR: Should "acute" be added before "myocardial infarction" (since abbreviation is AMI)? Also check at first mention in main text (AMI) without adverse effects. In a percutaneous pig model of reperfused AMI, a single intracoronary administration of antagomir-92a encapsulated in specific microspheres (9 μm poly-d,-lactide-co-glycolide [PLGA]) inhibited miR-92a in a local, selective, and sustained manner (n=3 pigs euthanized 1, 3, and 10 days after treatment; 8×, 2×, and 5×-fold inhibition at 1, 3, and 10 days). Downregulation of miR-92a resulted in significant vessel growth (n=27 adult minipigs randomly allocated to blind receive encapsulated antagomir-92a, encapsulated placebo, or saline [n=8, 9, 9]; P =0.001), reduced regional wall-motion dysfunction (P =0.03), and prevented adverse remodeling in the infarct area 1 month after injury (P =0.03). Intracoronary injection of microspheres had no significant adverse effect in downstream myocardium in healthy pigs (n=2), and fluorescein isothiocyanate albumin-PLGA microspheres were not found in myocardium outside the left anterior descending coronary artery territory (n=4) or in other organs (n=2). Early single intracoronary administration of encapsulated antagomir-92a in an adult pig model of reperfused AMI prevents left ventricular remodeling with no local or distant adverse effects, emerging as a promising therapeutic approach to translate to patients who suffer a large AMI. |