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Selective FPR2 Agonism Promotes a Proresolution Macrophage Phenotype and Improves Cardiac Structure-Function Post Myocardial Infarction.
García, Ricardo A; Lupisella, John A; Ito, Bruce R; Hsu, Mei-Yin; Fernando, Gayani; Carson, Nancy L; Allocco, John J; Ryan, Carol S; Zhang, Rongan; Wang, Zhaoqing; Heroux, Madeleine; Carrier, Marilyn; St-Onge, Stéphane; Bouvier, Michel; Dudhgaonkar, Shailesh; Nagar, Jignesh; Bustamante-Pozo, Moises M; Garate-Carrillo, Alejandra; Chen, Jian; Ma, Xiuying; Search, Debra J; Dierks, Elizabeth A; Kick, Ellen K; Wexler, Ruth R; Gordon, David A; Ostrowski, Jacek; Wurtz, Nicholas R; Villarreal, Francisco.
Afiliação
  • García RA; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Lupisella JA; Department of Medicine, University of California-San Diego, San Diego, California, USA.
  • Ito BR; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Hsu MY; Department of Medicine, University of California-San Diego, San Diego, California, USA.
  • Fernando G; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Carson NL; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Allocco JJ; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Ryan CS; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Zhang R; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Wang Z; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Heroux M; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Carrier M; Institute for Research in Immunology and Cancer, Université de Montréal, Montreal, Quebec, Canada.
  • St-Onge S; Institute for Research in Immunology and Cancer, Université de Montréal, Montreal, Quebec, Canada.
  • Bouvier M; Institute for Research in Immunology and Cancer, Université de Montréal, Montreal, Quebec, Canada.
  • Dudhgaonkar S; Institute for Research in Immunology and Cancer, Université de Montréal, Montreal, Quebec, Canada.
  • Nagar J; Biocon Bristol Myers Squibb Research Center, Bangalore, India.
  • Bustamante-Pozo MM; Biocon Bristol Myers Squibb Research Center, Bangalore, India.
  • Garate-Carrillo A; Department of Medicine, University of California-San Diego, San Diego, California, USA.
  • Chen J; Department of Medicine, University of California-San Diego, San Diego, California, USA.
  • Ma X; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Search DJ; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Dierks EA; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Kick EK; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Wexler RR; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Gordon DA; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Ostrowski J; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Wurtz NR; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
  • Villarreal F; Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.
JACC Basic Transl Sci ; 6(8): 676-689, 2021 Aug.
Article em En | MEDLINE | ID: mdl-34466754
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 ß-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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: JACC Basic Transl Sci Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: JACC Basic Transl Sci Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Estados Unidos