title: SR-BI mediates high density lipoprotein (HDL)-induced anti-inflammatory effect in macrophages.
abstract: High density lipoprotein (HDL) receptor, scavenger receptor class B, type I (SR-BI), mediates selective cholesteryl ester uptake from lipoproteins into the liver as well as cholesterol efflux from macrophages to HDL. Recently, strong evidence has demonstrated the anti-inflammatory effect of HDL, although the mechanism of action is not fully understood. In this study, we showed that the anti-inflammatory effects of HDL are dependent on SR-BI expression in THP-1 macrophages. Consistent with earlier findings, pretreatment of macrophages with HDL abolished LPS-induced TNFα production. HDL also inhibited LPS-induced NF-κB activation. In addition, knockdown of SR-BI or inhibition of SR-BI ligand binding abolished the anti-inflammatory effect of HDL. SR-BI is a multi-ligand receptor that binds to modified lipoproteins as well as native HDL. Since modified lipoproteins have pro-inflammatory properties, it is unclear whether SR-BI activated by modified HDL has an anti- or pro-inflammatory effect. Glycated HDL induced NF-κB activation and cytokine production in macrophages in vitro, suggesting a pro-inflammatory effect for modified HDL. Moreover, inhibition of SR-BI function or expression potentiated glycated HDL-induced TNF-α production, suggesting an anti-inflammatory effect for SR-BI. In conclusion, SR-BI plays an important function in regulating HDL-mediated anti-inflammatory response in macrophages.
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Republic of Korea; Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Republic of Korea; BK21Plus Program Serum Biomedical Research and Education Team, Yeungnam University, Gyeongsan 712-749, Republic of Korea.
authors.forename: Gyun Jee
authors.initials: GJ
authors.lastname: Song
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Republic of Korea; Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Republic of Korea; BK21Plus Program Serum Biomedical Research and Education Team, Yeungnam University, Gyeongsan 712-749, Republic of Korea.
authors.forename: Seong-Min
authors.initials: SM
authors.lastname: Kim
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Republic of Korea; Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Republic of Korea; BK21Plus Program Serum Biomedical Research and Education Team, Yeungnam University, Gyeongsan 712-749, Republic of Korea.
authors.forename: Ki-Hoon
authors.initials: KH
authors.lastname: Park
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Republic of Korea; Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Republic of Korea; BK21Plus Program Serum Biomedical Research and Education Team, Yeungnam University, Gyeongsan 712-749, Republic of Korea.
authors.forename: Jihoe
authors.initials: J
authors.lastname: Kim
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Republic of Korea; Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Republic of Korea; BK21Plus Program Serum Biomedical Research and Education Team, Yeungnam University, Gyeongsan 712-749, Republic of Korea.
authors.forename: Inho
authors.initials: I
authors.lastname: Choi
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Republic of Korea; Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Republic of Korea; BK21Plus Program Serum Biomedical Research and Education Team, Yeungnam University, Gyeongsan 712-749, Republic of Korea. Electronic address: chok@yu.ac.kr.
authors.forename: Kyung-Hyun
authors.initials: KH
authors.lastname: Cho
mesh_terms: D000893:Anti-Inflammatory Agents / Q000378:metabolism*; D018955:CD36 Antigens / Q000378:metabolism*; D006031:Glycosylation; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism*; D008954:Models, Biological; D015854:Up-Regulation
chemical_list: D000893:Anti-Inflammatory Agents; D018955:CD36 Antigens; D008075:Lipoproteins, HDL
keywords: Anti-inflammation; ApoA-I; Glycated HDL; HDL; Macrophages; SR-BI