Unknown

Dataset Information

0

Selective FPR2 Agonism Promotes a Proresolution Macrophage Phenotype and Improves Cardiac Structure-Function Post Myocardial Infarction.

ABSTRACT: Dysregulated inflammation following myocardial infarction (MI) leads to maladaptive healing and remodeling. The study characterized and evaluated a selective formyl peptide receptor 2 (FPR2) agonist BMS-986235 in cellular assays and in rodents undergoing MI. BMS-986235 activated G proteins and promoted β-arrestin recruitment, enhanced phagocytosis and neutrophil apoptosis, regulated chemotaxis, and stimulated interleukin-10 and monocyte chemoattractant protein-1 gene expression. Treatment with BMS-986235 improved mouse survival, reduced left ventricular area, reduced scar area, and preserved wall thickness. Treatment increased macrophage arginase-1 messenger RNA and CD206 receptor levels indicating a proresolution phenotype. In rats following MI, BMS-986235 preserved viable myocardium, attenuated left ventricular remodeling, and increased ejection fraction relative to control animals. Therefore, FPR2 agonism improves post-MI healing, limits remodeling and preserves function, and may offer an innovative therapeutic option to improve outcomes.

SUBMITTER: Garcia RA 

PROVIDER: S-EPMC8385569 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

Dysregulated inflammation following myocardial infarction (MI) leads to maladaptive healing and remodeling. The study characterized and evaluated a selective formyl peptide receptor 2 (FPR2) agonist BMS-986235 in cellular assays and in rodents undergoing MI. BMS-986235 activated G proteins and promoted β-arrestin recruitment, enhanced phagocytosis and neutrophil apoptosis, regulated chemotaxis, and stimulated interleukin-10 and monocyte chemoattractant protein-1 gene expression. Treatment with B  ...[more]

Similar Datasets

Unknown YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction.
| S-EPMC7735680 | biostudies-literature
Transcriptomics YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction
2020-10-02 | GSE158889 | GEO
Unknown Long-Term Administration of Eicosapentaenoic Acid Improves Post-Myocardial Infarction Cardiac Remodeling in Mice by Regulating Macrophage Polarization.
| S-EPMC5523759 | biostudies-literature
Unknown Micro RNA-411 Expression Improves Cardiac Phenotype Following Myocardial Infarction in Mice.
| S-EPMC9617134 | biostudies-literature
Unknown Adenosine kinase promotes post-infarction cardiac repair by epigenetically maintaining reparative macrophage phenotype.
| S-EPMC10420407 | biostudies-literature
Unknown Drug-based mobilisation of mesenchymal stem/stromal cells improves cardiac function post myocardial infarction.
| S-EPMC10655717 | biostudies-literature
Unknown Thymic stromal lymphopoietin modulates T cell response and improves cardiac repair post-myocardial infarction.
| S-EPMC11655303 | biostudies-literature
Unknown Metabolic Modulation of Macrophage Function Post Myocardial Infarction.
| S-EPMC7338762 | biostudies-literature
Unknown MAIR-II deficiency ameliorates cardiac remodelling post-myocardial infarction by suppressing TLR9-mediated macrophage activation.
| S-EPMC7753988 | biostudies-literature
Unknown Systemic and Cardiac Depletion of M2 Macrophage through CSF-1R Signaling Inhibition Alters Cardiac Function Post Myocardial Infarction.
| S-EPMC4583226 | biostudies-literature