Figure 6
ACE2 activated Akt through the ATP/P2 receptor/CaM signal pathway.
(A) The intracellular and extracellular ATP levels in ACE2-overexpressing HepG2 cells. (B) ACE2-induced Akt activation was inhibited by the IP3R antagonist (2-APB), the ATP receptor P2 antagonist (PPADS) and the CaM antagonist (CPZ). Infected HepG2 cells were treated with 2-APB (10 μM), PPADS (50 μM) or CPZ (100 μM) for 1 hour before pAkt levels was measured. The data are presented as the mean ± SD of n = 3 independent experiments in HepG2 cells. *P < 0.05 versus control cells, #P < 0.05 versus Ad-ACE2 infected cells without 2-APB, PPAD or CPZ treatment (n = 3). (C) ACE2-induced Akt activation was partially dependent on the presence of extracellular calcium. Infected cells were treated with calcium free medium HANK’S for 2 hours before pAkt levels were assayed. The data are presented as the mean ± SD of n = 3 independent experiments in HepG2 cells. *P < 0.05 versus control cells; #P < 0.05 versus Ad-ACE2 infected cells with calcium (n = 3).
