Angiotensin II modulates THP-1-like macrophage phenotype and inflammatory signatures via angiotensin II type 1 receptor
Proinflammatory cytokine
DOI:
10.3389/fcvm.2023.1129704
Publication Date:
2023-08-25T11:53:38Z
AUTHORS (8)
ABSTRACT
Angiotensin II (Ang II) is a major component of the renin–angiotensin or renin–angiotensin–aldosterone system, which main element found to be involved in cardiopathology. Recently, long-term metabolomics studies have linked high levels angiotensin plasma inflammatory conditions such as coronary heart disease, obesity, and type 2 diabetes. Monocyte/macrophage cellular function phenotype orchestrate response various pathological conditions, most notably cardiometabolic disease. An activation Ang system usually associated with inflammation cardiovascular disease; however, direct effect on monocyte/macrophages has still not been well elucidated. Herein, we evaluated effects THP-1-derived macrophages. stimulated expression markers monocyte/macrophage cell differentiation (e.g., CD116), adhesion, cell–cell interaction, chemotaxis, phagocytosis (CD15, CD44, CD33, CD49F). Yet, increased proinflammatory (HLA-DR, TNF-α, CD64, CD11c, CD38) decreased CD206 (mannose receptor), an M2 marker. Moreover, induced cytosolic calcium overload, reactive oxygen species, arrested cells G1 phase. Most these were via 1 receptor (AT1R). Collectively, our results provide new evidence support diseases.
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