ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

Macrophage, a highly plastic population, is widely distributed. Macrophage functions are settled and acquired polarization programs in response to microenvironmental signals and involved in many inflammatory disorders, such as experimental autoimmune myocarditis (EAM). Phenotypic and functional changes in macrophage are considered as an important determinant of disease progression and/or regression. Angiotensin II (ANG II), as a powerful proinflammatory factor, plays critical roles in inflammatory diseases and macrophage recruitment. It remains unclear whether ANG II contributed to the functional skewing of cardiac infiltrated monocytes/macrophage and involved in EAM development. Therefore, the present work was to address the above questions. Our data showed that ANG II contributed to CD11b⁺ Ly6C^hi (CD11b⁺ Ly6G^- Ly6C⁺ ) cells reprogramming into M1-like macrophage through Erk1/2 or p38/Stat3 pathway and the reprogramming M1-like cells promoted Th17 cells expansion; abrogation of ANG II-AT₁ R axis significantly ameliorated cardiac injury. The present work first demonstrated a novel immune regulation role of ANG II; ANG II, as a powerful immune factor, promoted CD11b⁺ Ly6C^hi inflammatory cells reprogramming into M1-like macrophage and involved in inflammatory disorders development; our results also indicated that ANG II may be a potential therapeutic target for inflammatory diseases.

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