LincRNA DYN‐LRB2‐2 upregulates cholesterol efflux by decreasing TLR2 expression in macrophages

This study is designed to determine whether lincRNA‐DYNLRB2‐2 could promote cholesterol efflux through regulating the expression of TLR2. THP‐1 and RAW264.7 cells were incubated with oxLDL for 48 h to induce the formation of foam cells, and ORO staining was performed and intracellular cholesterol contents were measured by HPLC assay. qRT‐PCR and Western blotting were performed to detect mRNA and protein expression levels, respectively. Lentiviral vector LV‐DYNLRB2‐2 and lincRNA‐DYNLRB2‐2 siRNA was constructed to explore its potential role. The cholesterol efflux was assessed by liquid scintillation counting. The effects of TRL2 were determined in apoE −/− mice that fed a high fat diet and were randomly divided into three groups and infected with LV‐Mock, LV‐Sh‐TRL2, or LV‐TRL2. Atherosclerosis was observed in the aortic sinus and the levels of cytokines and serum biochemical parameters were measured. Ox‐LDL induced foam cell formation in the THP‐1 and RAW264.7 cells. LincRNA DYN‐LRB2‐2 was upregulated in oxLDL‐treated THP‐1 and Raw264.7 cells. LincRNA‐DYNLRB2‐2 plays important role in regulating the cholesterol efflux, ABCA1 expression level and anti‐inflammatory processes in THP‐1 and RAW264.7 cells. Further study indicated that lincRNA‐DYNLRB2‐2 negatively regulated TRL2 expression and TRL2 overexpression reversed the effects of lincRNA‐DYNLRB2‐2 on cholesterol efflux and ABCA1 expression level in THP‐1 and RAW264.7 cells. Besides, we found TRL2 plays important role in lipid accumulation, plaque formation and regulating serum inflammatory cytokines level in apoE −/− mice with a high fat diet. LincRNA DYN‐LRB2‐2 upregulates cholesterol efflux by decreasing TLR2 expression in macrophages.