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Oncostatin M promotes infarct repair and improves cardiac function after myocardial infarction

ABSTRACT: Myocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide. The immune response plays a central role in post-MI cardiac repair. A growing body of evidence suggests that oncostatin M (OSM), a pleiomorphic cytokine of the interleukin (IL)-6 family, participates in the cardiac healing and remodeling process. However, previous studies have shown inconsistent results, and the exact mechanisms underlying this process have not yet been fully elucidated. We verified whether OSM is involved in the healing process and cardiac remodeling after MI and sought to explore its potential mechanisms. Our data implied OSM’s role in facilitating the post-MI healing process in mice, manifested by improved cardiac functional performance and a reduction in fibrotic changes. Furthermore, our flow cytometry analysis revealed that OSM influences the dynamics of cardiac monocytes and macrophages. In mice with a blunted C-X-C motif receptor (CCR)2 signaling pathway, OSM reserved its protective roles and polarized cardiac macrophages toward a reparative phenotype. Moreover, OSM reduced the number of matrix metalloproteinase (MMP)-9+ immune cells and increased the number of tissue inhibitor of metalloproteinase (TIMP)-1+ immune cells in the infarct area, mitigating the maladaptive remodeling following MI. These findings demonstrate that OSM favorably modulates cardiac remodeling, partially by accelerating the shift in the cardiac macrophage phenotype from M1 to M2 and by correcting the MMP-9 and TIMP-1 balance.

SUBMITTER: Han H

PROVIDER: S-EPMC8581943 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Myocardial infarction (MI) causes irreversible damage to the heart muscle, seriously threatening the lives of patients. Injectable hydrogels have attracted extensive attention in the treatment of MI. By promoting the coupling of mechanical and electrical signals between cardiomyocytes, combined with synergistic therapeutic strategies targeting the pathological processes of inflammation, proliferation, and fibrotic remodeling after MI, it is expected to improve the therapeutic effect. In this study, a pH/ROS dual-responsive injectable hydrogel was developed by modifying xanthan gum and gelatin with reversible imine bond and boronic ester bond double crosslinking. By encapsulating polydopamine-rosmarinic acid nanoparticles to achieve on-demand drug release in response to the microenvironment of MI, thereby exerting anti-inflammatory, anti-apoptotic, and anti-fibrosis effects. By adding conductive composites to improve the conductivity and mechanical strength of the hydrogel, restore electrical signal transmission in the infarct area, promote synchronous contraction of cardiomyocytes, avoid induced arrhythmias, and induce angiogenesis. Furthermore, the multifunctional hydrogel promoted the expression of cardiac-specific markers to restore cardiac function after MI. The in vivo and in vitro results demonstrate the effectiveness of this synergistic comprehensive treatment strategy in MI treatment, showing great application potential to promote the repair of infarcted hearts. Graphical abstract Image 1 Highlights • An injectable self-healing conductive hydrogel with pH/ROS dual-responsive drug release was prepared for the treatment of MI.• The OGDPR hydrogel has conductivity (6.27 × 10−4 S/cm) and elastic modulus (45.35 kPa) matching those of the natural heart.• The biocompatible hydrogel can resist oxidation, promote macrophage polarization and tube formation of endothelial cells.• The hydrogel can protect cardiac function, reduce arrhythmia susceptibility, and reduce infarct size and fibrosis after MI.• The hydrogel can reduce apoptosis and inflammation, and promote angiogenesis and the expression of cardiac-specific markers.

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Oncostatin M promotes infarct repair and improves cardiac function after myocardial infarction

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