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. 2013 Oct 21;8(10):e78322. doi: 10.1371/journal.pone.0078322

Figure 3. ER stress plays a key role in TGRL modulation of TNFα-stimulated VCAM-1 expression.

Figure 3

A-B: ER stress inhibition dose-dependently reduced TNFα-induced VCAM-1 expression but did not affect ICAM-1 expression. HAEC were conditioned for 4 hr (A) or 2 hr (B) with TNFα (0.3 ng/ml) and 4-phenyl butyric acid (4-PBA) at different doses (0, 0.3, 1, or 3 mM, with 1 hr pretreatment). VCAM-1 and ICAM-1 protein or mRNA expression analyzed by flow cytometry (A) or quantitative RT-PCR (B). n=3-5. *P<0.05, **P<0.01 from TNFα stimulated alone. (C) ER stress inhibition abolished TGRL modulation of TNFα-stimulated VCAM-1 expression. HAEC were treated for 4 hr with TNFα (0.3 ng/ml) alone or simultaneously with pro- or anti-atherogenic TGRL (10 mg ApoB/dL) in the presence (1 mM, 1 hr pretreatment and 4 hr co-treatment) or absence of 4-PBA. n=4-7. ***P<0.001, **P<0.01 from TNFα-stimulated alone. ns, not significant.