NIL10: a new IL10-receptor binding nanoparticle that induces cardiac protection in mice and pigs subjected to acute myocardial infarction through STAT3/NF-κB activation

(1) Background: Early response after acute myocardial infarction (AMI) prevents extensive cardiac necrosis, in which inflammation resolution, including expression of anti-inflammatory interleukin-10 (IL-10), may play a key role. (2) Methods: We synthesized NIL10, a micelle-based nanoparticle, to tar...

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Detalles Bibliográficos
Autores: Tesoro, Laura, Hernández, Ignacio, Ramírez Carracedo, Rafael, Díaz Mata, Javier, Alcharani, Nunzio, Jiménez Guirado, Beatriz, Ovejero Paredes, Karina, Fillice, Marco, Zamorano Gómez, José Luís|||0000-0002-0487-1749, Saura Redondo, Marta|||0000-0002-3977-6581, Zaragoza Sánchez, Carlos, Botana, Laura
Tipo de recurso: artículo
Fecha de publicación:2022
País:España
Institución:Universidad de Alcalá (UAH)
Repositorio:e_Buah Biblioteca Digital Universidad de Alcalá
Idioma:inglés
OAI Identifier:oai:ebuah.uah.es:10017/63461
Acceso en línea:http://hdl.handle.net/10017/63461
https://dx.doi.org/10.3390/pharmaceutics14102044
Access Level:acceso abierto
Palabra clave:Acute myocardial infarction
Interleukin-10
Nanoparticles
STAT-3
NF-κB
Medicina
Medicine
Descripción
Sumario:(1) Background: Early response after acute myocardial infarction (AMI) prevents extensive cardiac necrosis, in which inflammation resolution, including expression of anti-inflammatory interleukin-10 (IL-10), may play a key role. (2) Methods: We synthesized NIL10, a micelle-based nanoparticle, to target IL-10 receptor in mice and pigs subjected to AMI. (3) Results: Administration of NIL10 induced cardiac protection of wild-type and IL-10 knockout mice and pigs subjected to AMI. Cardiac protection was not induced in IL-10-receptor null mice, as shown by a significant recovery of cardiac function, in which inflammatory foci and fibrosis were strongly reduced, together with the finding that resolving M2-like macrophage populations were increased after day 3 of reperfusion. In addition, anti-inflammatory cytokines, including IL-4, IL-7, IL-10, IL-13, IL-16, and IL-27 were also elevated. Mechanistically, NIL10 induced activation of the IL-10 receptor/STAT-3 signaling pathway, and STAT3-dependent inhibition of nuclear translocation of pro-inflammatory NF-ĸB transcription factor. (4) Conclusions: Taken together, we propose using NIL10 as a novel therapeutic tool against AMI-induced cardiac damage.

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