Hypoxia regulates osteopontin expression of mature dendritic cells via adenosine 2 receptor
10.3760/cma.j.issn.0254-5101.2011.02.003
- VernacularTitle:乏氧通过腺苷A2受体调节人成熟树突状细胞骨桥蛋白的表达
- Author:
Weixu HU
;
Jintang SUN
;
Qianqian SHAO
;
Alei FENG
;
Yun ZHANG
;
Qi XIE
;
Meixiang YANG
;
Chunyan JI
;
Xun QU
- Publication Type:Journal Article
- Keywords:
Mature dendritic cells;
Adenosine A2 receptor;
Osteopontin;
Hypoxia
- From:
Chinese Journal of Microbiology and Immunology
2011;31(2):108-112
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of hypoxia regulate osteopontin (OPN) secreting by mature dendritic cells (mDCs). Methods CD14 + cells were enriched using anti-CD14 immunomagnetic beads, for inducing to mDCs, CD14 + cells were cultured with GM-CSF and IL-4 in hypoxia or normoxiain vitro. Concentration of OPN and TGF-β1 in supernatant were detected by sandwich ELISA, OPN mRNA detected by RT-PCR. Approach regulating function of A2 R in expressing of OPN by mDCs by using NECA (surrogate of adenosine), A2R agonist (CGS21680), A2R antagonist (SCH58261) and investigate role of TGF-β1 in this process by using rhTGF-β1 and anti-TGF-β1 Ab. Results Hypoxia inreased the level of OPN and OPN mRNA in mDCs, and this effect could be reversed by A2 R antagonist. Under normoxia,both NECA and A2R agonist (CGS21680) could upregulate the level of OPN and OPN mRNA in mDCs significantly, but this positive effect could be reversed by A2 R antagonist. A2 R played a role in regulating TGF-β1, and confirmed TGF-β1 involved in regulation of OPN by using rhTGF-β1 and anti-TGF-β1 Ab. Conclusion High adenosine induce the generation of TGF-β1 through the A2R on mDCs, and then TGF-β1 raise the OPN secreting by mDCs.
