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. 2013 Jun 21;305(4):H484–H493. doi: 10.1152/ajpheart.00642.2012

Fig. 3.

Fig. 3.

LS-induced upregulation of KCa3.1 and KCa2.3 expression is mediated by CaMKK-dependent Akt activation. A and B: HCAECs were exposed to LS for 24 h in the absence or presence of compound C (an AMPK inhibitor), KN-62 (a CaMK inhibitor), or Akt inhibitor IV. Compound C tended to reduce LS-induced upregulation of KCa3.1 mRNA expression (A) but did not change LS induction of KCa2.3 expression (B) (n = 9). KN-62 had no effect on the upregulation of KCa3.1 and KCa2.3 mRNA expression (n = 7–8). Akt inhibition completely blocked LS-induced upregulation of both KCa3.1 and KCa2.3 expression. C: LS-induced increase in KCa2.3 and KCa3.1 protein expression levels was suppressed by Akt inhibition. Top: a representative image of immunoblots. Bottom: the summaries of densitometric analysis of KCa3.1 and KCa2.3 signals (n = 3). D: Akt inhibitor IV abolished the phosphorylation of Akt at Ser473 in HCAECs exposed to 60-min LS (top). Levels of phospho-Akt (Ser473) were suppressed after inhibiting CaMKK with STO-609 in ECs exposed to 15 min of LS (bottom). Phosphorylation of Akt at Thr308 was not observed in ECs under ST or LS condition. #Signficant difference vs. LS (P < 0.05).