Effect of oxidized low-density lipoprotein on dendritic cells-induced inflammation in microenvironment of myocardial infarction

Objective：To explore the induction of maturation, migration, and inflammation of dendritic cells (DCs) after treatment with angiotensin (Ang)Ⅱ via oxidized low-density lipoprotein (ox-LDL), and its corresponding signaling pathway. Methods：Bone marrow cells from C57BL/6J WT mice were differentiated into DCs. After adding supernatant of necrotic cardiomyocyte cells, DCs were treated with either AngⅡalone or in combination with ox-LDL for 48 h. CD83 and CD86 were measured via flow cytometry, while cytokines and chemokine levels were measured by the qPCR or ELISA. Nuclear factor κB (NF-κB) and IκB phosphorylation were detected by Western blotting. The expressions of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), myeloid differentiation factor 88 (MyD88), and Toll-like receptor (TLR)4 were detected by Western blotting. Results：Ox-LDL could further up-regulate the maturity marker CD83 and CD86 in DCs on the basis of AngⅡtreatment. The expressions of inflammatory factors and chemokines, as well as phosphorylation of NF-κB and IκB were upregulated (P<0.05). The expression of LOX-1, phosphorylation of interleukin-1 receptor associated kinase (IRAK)-4 and the activation of TLR4/MyD88 signaling pathway were further enhanced by ox-LDL (P<0.05). Conclusions：The immune maturation, migration, and inflammation of DCs treated with AngⅡcould be further induced by ox-LDL, possibly via the LOX-1-TLR4-MyD88 signaling pathway.