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. 2022 Mar 28;13:815301. doi: 10.3389/fphys.2022.815301

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Copyright © 2022 Zhong, Zhao, Xie, Qi, Li, Jia, Zhang and Lu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Cx43 hyperphosphorylation and lateralization induced by 18β-GA produce an abnormal QRS complex. (A) 18β-GA (0.5, 1, and 4 μm) perfusion (80 min) produced abnormal QRS duration of isolated rat hearts. Light gray box: QRS duration of isolated heart after stabilization; light green box: QRS duration of isolated heart after 40-min of perfusion; light red box: QRS duration of isolated heart after 80-min of perfusion. (B–D) Statistical data changes of QRS duration, QRS amplitude, and HR. n = 5 for each group. (E) Western blot images of pS368Cx43 and Cx43 in the control and 18β-GA-treated rats’ cardiac ventricles. The level of pS368Cx43 and Cx43 was normalized to GAPDH. (F) Immunohistochemical analysis of Cx43 and pS368Cx43 expression and redistribution (Bar = 20 μm), and corresponding statistical data of Cx43⁺ and pS368Cx43⁺ cells ratio. Error bars represent mean ± SD. *p < 0.05 vs. control; **p < 0.01 vs. control; ***p < 0.001 vs. control.