Murao, Atsushi; Tan, Chuyi; Jha, Alok; Wang, Ping; Aziz, Monowar published the artcile< Exosome-mediated eCIRP release from macrophages to induce inflammation in sepsis>, Application In Synthesis of 6823-69-4, the main research area is inflammation sepsis exosome extracellular cold inducible RNA binding protein; cytokines; eCIRP; exosomes; macrophage; neutrophil; sepsis.
Extracellular cold-inducible RNA-binding protein (eCIRP) is an important damage-associated mol. pattern (DAMP). Despite our understanding of the potentially harmful effects of eCIRP in sepsis, how eCIRP is released from cells remains elusive. Exosomes are endosome-derived extracellular vesicles, which carry proteins, lipids, and nucleic acids to facilitate intercellular communication and several extracellular functions. We hypothesized that eCIRP is released via exosomes to induce inflammation in sepsis. Exosomes isolated from the supernatants of LPS-treated macrophage culture and serum of endotoxemia and polymicrobial sepsis mice showed high purity, as revealed by their unique median sizes ranging between 70 and 126 nm in diameter eCIRP levels of the exosomes were significantly increased after LPS treatment in the supernatants of macrophage culture, mouse serum, and cecal ligation and puncture (CLP)-induced sepsis mouse serum. Protease protection assay demonstrated the majority of eCIRP was present on the surface of exosomes. Treatment of WT macrophages and mice with exosomes isolated from LPS-treated WT mice serum increased TNFα and IL-6 production However, treatment with CIRP-/- mice serum exosomes significantly decreased these levels compared with WT exosome-treated conditions. CIRP-/- mice serum exosomes significantly decreased neutrophil migration in vitro compared with WT exosomes. Treatment of mice with serum exosomes isolated from CIRP-/- mice significantly reduced neutrophil infiltration into the peritoneal cavity. Our data suggest that eCIRP can be released via exosomes to induce cytokine production and neutrophil migration. Thus, exosomal eCIRP could be a potential target to inhibit inflammation.
Frontiers in Pharmacology published new progress about Binding energy. 6823-69-4 belongs to class imidazoles-derivatives, and the molecular formula is C30H30Cl2N6O2, Application In Synthesis of 6823-69-4.
Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem