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. 2010 Mar 18;59(6):1386–1396. doi: 10.2337/db09-1637

FIG. 4.

FIG. 4.

AMPK activation by AICAR suppresses HOG-LDL–induced ER stress and protects SERCA activity. BAECs were treated with HOG-LDL, with or without AICAR preincubation (1 mmol/l, 30 min). A: AICAR increases AMPK phosphorylation at Thr172 in BAECs. n = 3. *P < 0.05 HOG-LDL-3 h vs. 0 h control; #P < 0.01 AICAR+HOG-LDL vs. HOG-LDL alone at times indicated. B: AICAR suppresses the rise of intracellular [Ca2+]i in BAECs at 6 h. n = 3. *P < 0.05 HOG-LDL vs. control or N-LDL; #P < 0.05 HOG-LDL+AICAR vs. HOG-LDL alone. C: AICAR suppresses HOG-LDL–induced ER stress in BAECs. n = 4. D: AICAR pretreatment inhibited NADPH oxidase activation by blocking p47 translocation. n = 3. *P < 0.05 HOG-LDL vs. N-LDL in cytosol and membrane portion; # and † indicate P < 0.05 AICAR pretreatment completely blocked p47 translocation by HOG-LDL in cytosol and membrane, respectively. E: AICAR protects SERCA activity under HOG-LDL treatment. n = 4. *P < 0.05 AICAR treatment vs. N-LDL or control samples; #P < 0.05 HOG-LDL vs. N-LDL or control; †P < 0.05 AICAR+HOG-LDL vs. HOG-LDL alone. F: Ratiometric measurement of intracellular Ca2+. BAECs were treated with 100 μg/ml N-LDL, 100 μg/ml HOG-LDL, and AICAR (pretreated for 30 min)+HOG-LDL for 6 h. Ratiometric measurement of intracellular Ca2+ was done as described in the “Research Design and Methods” section. The small arrows indicate the timing for cytosolic Ca2+ return to its homeostasis. n = 6.