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. Author manuscript; available in PMC: 2018 Aug 29.
Published in final edited form as: Circulation. 2017 Jun 22;136(9):834–848. doi: 10.1161/CIRCULATIONAHA.116.024307

Figure 3. Cx43 mediated intercellular transmission of Ca2+ influence the ACM redifferentiation.

Figure 3

A: The percentage of sarcomere+ ACMs in co-culture at day 7 with Ca2+ blocker BAPTA-AM and thapsigargin. B: The property of Ca2+ transients in ACMs cocultured with NRVMs over-expressing Ca2+ regulating protein SERCA2a or NCX1. The graph bars represent [Ca2+]i transient amplitude (change from diastolic [Ca2+]i to peak systolic [Ca2+]i) of redifferentiated ACMs and their coupled NRVMs. C: The percentage of ACMs with sarcomere+ (C1) or spontaneous beating (C2) in co-cultures with NRVMs overexpressing SERCA2a or NCX1 at day 7. D: The percentage of sarcomere+ ACMs in co-cultures at day 7 with Cx43 manipulation. E: The percentage of sarcomere+ ACMs in co-cultures at day 7 with Cx43 manipulation under hypoxia. N=8–10; * p<0.05 vs. control or scramble or vector; # p<0.05 vs. vector+hypoxia.