Wang Yunlong, Wang Yanhui, Jia Shaoyou, Dong Qingzhe, Chen Yuanbin, Lu Shulai, Hou Lin
Biological Specimen Bank, The Affiliated Hospital of Qingdao University, Qingdao, China.
Department of Biochemistry, Medical College, Qingdao University, Qingdao, Shandong, China.
Biosci Rep. 2017 Feb 3;37(1). doi: 10.1042/BSR20160398. Print 2017 Feb 28.
Activating transcription factor 3 (ATF3) is a TLR-induced repressor that plays an important role in the inhibition of specific inflammatory signals. We previously constructed recombinant high density lipoproteins (rHDL) (including rHDL, rHDL, rHDL and rHDL) and found that rHDL had a strong anti-inflammatory ability. In the present study, we investigate the roles of recombinant apolipoprotein A-I (ApoA-I) (rHDL) and its cysteine mutant HDLs (rHDL, rHDL and rHDL) on ATF3 function in RAW264.7 cells stimulated by lipopolysaccharide. Our results showed that compared with the LPS group, rHDL can decrease the level of TNF-α and IL-6, whereas rHDL increases their expression levels. RT-PCR and Western blotting results showed that compared with the LPS group, rHDL, rHDL and rHDL can markedly increase the expression level of ATF3, whereas the level of ATF3 decreases in the rHDL group. In summary, the different anti-inflammatory mechanisms of the ApoA-I cysteine mutants might be associated with the regulation of ATF3 level.