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Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Drug+Des+Devel+Ther 2017 ; 11 (ä): 617-27 Nephropedia Template TP
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?3-Adrenoceptor activation upregulates apolipoprotein A-I expression in HepG2 cells, which might further promote cholesterol efflux from macrophage foam cells #MMPMID28424539
Gao Xq; Li Yf; Jiang Zl
Drug Des Devel Ther 2017[]; 11 (ä): 617-27 PMID28424539show ga
Objective: The aim of this study was to explore the effects of ?3-adrenoceptor (?3-AR) activation on HepG2 cells and its influence on cholesterol efflux from macrophage foam cells. Materials and methods: HepG2 cells were cultured and treated with the ?3-AR agonist, BRL37344, and antagonist, SR52390A, and the expression of apolipoprotein (Apo) A-I, ApoA-II, ApoB, and ?3-AR in the supernatants and cells was determined. The expression of peroxisome proliferator-activated receptor (PPAR) ? and PPAR? in the HepG2 cells was also assessed. Next, using the RAW264.7 macrophage foam cell model, we also assessed the influence of the HepG2 cell supernatants on lipid efflux. The cholesterol content of the foam cells was also measured, and the cholesterol efflux from the macrophages was examined by determining 3H-labeled cholesterol levels. Expression of ATP-binding cassette transporter (ABC) A1 and ABCG1 of the macrophage foam cells was also assessed. Results: ?3-AR activation increased ApoA-I expression in both the HepG2 cells and the supernatants; PPAR? expression was upregulated, but PPAR? expression was not. Treatment with GW9662 abolished the increased expression of ApoA-I induced by the ?3-AR agonist. The HepG2 cell supernatants decreased the lipid accumulation and increased the cholesterol efflux from the macrophage foam cells. ABCA1 expression, but not ABCG1 expression, increased in the macrophage foam cells treated with BRL37344-treated HepG2 cell supernatants. Conclusion: Activation of ?3-AR in HepG2 cells upregulates ApoA-I expression, which might further promote cholesterol efflux from macrophage foam cells. PPAR? might be required for the induction of ApoA-I expression.