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PPAR‐γ agonist inhibits Ang II‐induced activation of dendritic cells via the MAPK and NF‐κB pathways
Author(s) -
Weiguo Zhu,
Hui Yan,
Shan Li,
Yun Zhang,
Wencheng Nie,
Fulin Yu,
Fangyan Fan,
Junhua Ge,
Jianhua Zhu
Publication year - 2009
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2009.100
Subject(s) - mapk/erk pathway , microbiology and biotechnology , signal transduction , nf κb , angiotensin ii , kinase , p38 mitogen activated protein kinases , agonist , chemistry , protein kinase a , receptor , biology , biochemistry
The renin‐angiotensin system exerts a profound regulatory effect on the functional features of dendritic cells (DCs), thus suggesting a new target of angiotensin II (Ang II) action in the immune system. This study analyzed whether peroxisome proliferator‐activated receptor‐gamma (PPAR‐γ) activation in DCs regulated Ang II‐induced activation of DCs and exploited the possible molecular mechanisms, especially focused on the signaling pathways of mitogen‐activated protein kinase (MAPK) and nuclear factor‐kappa B (NF‐κB). Ang II stimulation of human monocyte‐derived DCs resulted in an intermediate state of DC maturation and function via modulating the balance of the negative or positive regulation of the signaling pathways of extracellular regulated kinase (ERK), p38 MAPK and NF‐κB, but not c‐Jun N‐terminal kinase (JNK). Moreover, pretreatment of DCs with the PPAR‐γ agonist pioglitazone reverted these effects of Ang II on DCs via suppression of the MAPK and NF‐κB signaling pathways at least in part. Collectively, our data support the notion that PPAR‐γ activation in human DCs inhibits the activation of DCs induced by Ang II, with which involves the regulation of MAPK and NF‐κB signaling pathways. These findings may support the important role of these mediators in the regulation of DC‐mediated inflammatory and immunologic processes.