Fig. 1.

Alleviation of endoplasmic reticulum (ER) stress mitigates palmitic acid (PA)-induced oxidized LDL receptor-1 (LOX-1) upregulation in THP-1 cells. A: Cells were treated with 200 μM PA, and ER stress markers were analyzed by Western blot. eIF2α, eukaryotic translation initiation factor 2α; JNK, c-JUN N-terminal kinase; CHOP, C/EBP homologous protein. B: Western blot analysis of ER stress markers in cells stimulated with PA for 6 h at the indicated concentrations. C: (upper) LOX-1 gene expression in cells stimulated with PA for 24 h at the indicated concentrations. LOX-1 expression was quantified by real-time PCR and normalized relative to 18S rRNA. Data are expressed as means ± SE of three independent experiments. * P < 0.05, ** P < 0.01 versus Cont (lower). Time course of changes in PA (200 μM)-induced LOX-1 upregulation. Data are averaged values from two experiments. D, E: Effects of 4-phenylbutyric acid (PBA), sodium tauroursodeoxycholate (TUDCA), and salubrinal on PA-induced LOX-1 upregulation. THP-1 cells were stimulated with 200 μM PA in the presence or absence of 4-phenylbutyric acid (PBA) (20 mM), TUDCA (2 mM), and salubrinal (40 μM). LOX-1 expression (D) and phosphorylation of protein kinase-like ER kinase (PERK) (E) were analyzed by real-time PCR and Western blot, respectively. Data in D are expressed as means ± SE of five independent experiments. ** P < 0.01 versus PA. F: Concentration-dependent inhibition of PA-induced LOX-1 induction by SP600125. Data are expressed as means ± SE of three independent experiments. ** P < 0.01 versus PA.