Skip to main content
. 2010 Dec 7;286(6):4912–4921. doi: 10.1074/jbc.M110.199729

FIGURE 1.

FIGURE 1.

ER stress preconditioning suppressed TNF-α-induced ICAM-1 and VCAM-1 expression in HREC. HREC were preincubated with 0.1 μg/ml tunicamycin (TM; A–G) or 10 nm thapsigargin (TG; H–J) for 8 h followed by exposure to 10 ng/ml TNF-α for 4h or 24 h. A, the mRNA level of ICAM-1 and VCAM-1 was measured by real-time RT-PCR in tunicamycin-preconditioned HREC after TNF-α treatment for 4 h. B and C, expression of ICAM-1 (B) and VCAM-1 (C) was analyzed by immunocytochemistry in tunicamycin-preconditioned HREC after TNF-α treatment for 24 h. Results show that ICAM-1 (B, a) and VCAM-1 (C, a) were expressed at low levels in unstimulated HREC but robustly increased after TNF-α treatment (B, b and C, b). Pretreatment with TM markedly inhibited TNF-α-induced ICAM-1 (B, c) and VCAM-1 (C, c) expression. D–G, expression of ICAM-1 (D) and VCAM-1 (F) was determined by Western blot analysis in tunicamycin-preconditioned HREC after TNF-α treatment for 4 and 24 h and semiquantified by densitometry (E and G). H–J, expression of ICAM-1 and VCAM-1 in thapsigargin-preconditioned HREC were detected by Western blot analysis after TNF-α treatment for 24 h and semiquantified by densitometry (I and J). **, p < 0.01 versus control and ‡, p < 0.01 versus TNF-α. Ctrl, control.