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. Author manuscript; available in PMC: 2017 Jan 1.

Published in final edited form as: Vascul Pharmacol. 2015 Jul 26;76:42–52. doi: 10.1016/j.vph.2015.07.011

HCAECs were maintained in EBM-2 alone (Control) or EBM-2 containing thapsigargin (“Thaps”, 1 μM) or tunicamycin (“Tun”, 10 μg/ml) in the presence or absence of the selective CAMKII inhibitor KN93 (“KN93”, 10 μM, panel A) or its inactive analogue KN92 (“KN92”, 10 μM, panel B) and then processed for in vitro TUNEL assay. P values for the differences between treatments with and without KN93 are shown. Differences between treatments with thapsigargin or tunicamycin and the control had P <0.001. All values are mean ± SEM (n=3). ns: not statistically significant. *P=0.011, **P=0.03, for the differences between thapsigargin vs. control and tunicamycin vs. control, respectively.

HCAECs were maintained in EBM-2 alone (Control) or EBM-2 containing thapsigargin (“Thaps”, 1 μM) or tunicamycin (“Tun”, 10 μg/ml) in the presence or absence of the selective CAMKII inhibitor KN93 (“KN93”, 10 μM, panel A) or its inactive analogue KN92 (“KN92”, 10 μM, panel B) and then processed for in vitro TUNEL assay. P values for the differences between treatments with and without KN93 are shown. Differences between treatments with thapsigargin or tunicamycin and the control had P <0.001. All values are mean ± SEM (n=3). ns: not statistically significant. *P=0.011, **P=0.03, for the differences between thapsigargin vs. control and tunicamycin vs. control, respectively.