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. Author manuscript; available in PMC: 2013 Aug 27.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2013 Jan 3;33(3):595–604. doi: 10.1161/ATVBAHA.112.300606

Figure 3.

Figure 3

AMP-activated protein kinase (AMPK) activation suppresses endoplasmic reticulum (ER) stress-potentiated myosin light chain (MLC) phosphorylation in cultured vascular smooth muscle cells (VSMCs). A and B, Immunoblots showing the levels of ER stress relative protein P-elf2α(s51), Grp78, and spliced XBP-1 in human smooth muscle cells (HSMCs) treated with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR; A) and metformin (B) after Tunicamycin incubation for 6 hours; n=5. *P<0.05, Tunicamycin vs vehicle; #P<0.05, Tunicamycin vs Tunicamycin plus AICAR or metformin. C and D, Effects of AICAR and metformin on Tunicamycin-induced MLC phosphorylation in VSMCs. VSMCs were incubated with indicated concentrations of Tunicamycin for 6 hours; n=5. *P<0.05 Tunicamycin vs vehicle; #P<0.05 Tunicamycin vs Tunicamycin plus AICAR or metformin. E and F, Effects of Tunicamycin on RhoA kinase. Confluent VSMCs were treated with tunicamycin for 4 hours (E) or 6 hours (F) with or without 4-phenyl butyric acid (4-PBA). After the incubation, cells were collected and GTP-bound RhoA was pull-down/detected by total RhoA antibody. The blot is representative of 5 blots from 5 independent experiments. Statistical analysis for A to C was performed using a 2-tailed Student t test between 2 groups.