Hemichannel‑mediated volume regulation contributes to IPC‑induced cardiomyocyte protection

  • Authors:
    • Wenying Wang
    • Dedong Zheng
    • Huiya Li
    • Jinhua Huang
    • Huijun Chen
    • Teng Ying
    • Jun Fang
    • Yukun Luo
  • View Affiliations

  • Published online on: December 21, 2018     https://doi.org/10.3892/etm.2018.7127
  • Pages: 1847-1854
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Abstract

Cx43 has been documented to be involved in ischemic preconditioning (IPC). However, the participation of Cx43‑formed hemichannels in IPC and the potential underlying mechanisms remain unclear. The present study focused on cardiomyocytes' volume regulation during IPC to investigate the role of hemichannels in the IPC‑induced cardioprotection. In the study, mice cardiomyocytes were respectively treated with a hemichannel blocker, octanol or 18a‑Glycyrrhizic acid (18a‑GA), and a Cx43‑silenced lentivirus. They were subsequently cultured in hypotonic solution to simulate ischemic reperfusion (SIR) and systemic ischemic preconditioning (SIP). Cell morphology and volumetric (area) change were detected by inverted microscopy at 30 min following the addition of hypotonic solution. Cardiomyocyte mortality was assessed by trypan blue stain assay. The analyses revealed that regardless of the treatments, hypotonic solution aggravated cell edema: Compared with the initial condition (the moment before the solution addition, 0 min), the volumetric area increased significantly 30 min later (for hypotonic+DMSO, 5,050±1,511 vs. 3,464±723 µm2; for hypotonic+scramble lentiviral vector, 5,517±1,128 vs. 2,331±536 µm2; P<0.05, respectively). Either treatment alleviated the edematous condition when a comparison was made between 30 min after the hypotonic addition and 0 min (for hypotonic+octanol, 2,990±765 vs. 2,821±773 µm2; for hypotonic+18a‑GA, 4,817±1,306 vs. 4,762±1,271 µm2; for hypotonic+Cx43‑silenced, 3,627±688 vs. 3,419±814 µm2; P>0.05 for all). Notably, results indicated that the SIP group had lower mortality rates compared with its SIR counterpart; the hypotonic+octanol, hypotonic+18a‑GA, and hypotonic+Cx43‑silenced group showed markedly‑declined mortality when compared with their respective control groups (respectively, 35.70±1.02, 30.76±2.20 vs. 53.58±2.14%; 30.89±2.37 vs. 54.12±2.55%; P<0.05 for all). The results suggest that ischemic preconditioning may provide cardioprotection by blocking the opening of the hemichannels and further mediating the volume regulation of cardiomyocytes.
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March-2019
Volume 17 Issue 3

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Spandidos Publications style
Wang W, Zheng D, Li H, Huang J, Chen H, Ying T, Fang J and Luo Y: Hemichannel‑mediated volume regulation contributes to IPC‑induced cardiomyocyte protection. Exp Ther Med 17: 1847-1854, 2019
APA
Wang, W., Zheng, D., Li, H., Huang, J., Chen, H., Ying, T. ... Luo, Y. (2019). Hemichannel‑mediated volume regulation contributes to IPC‑induced cardiomyocyte protection. Experimental and Therapeutic Medicine, 17, 1847-1854. https://doi.org/10.3892/etm.2018.7127
MLA
Wang, W., Zheng, D., Li, H., Huang, J., Chen, H., Ying, T., Fang, J., Luo, Y."Hemichannel‑mediated volume regulation contributes to IPC‑induced cardiomyocyte protection". Experimental and Therapeutic Medicine 17.3 (2019): 1847-1854.
Chicago
Wang, W., Zheng, D., Li, H., Huang, J., Chen, H., Ying, T., Fang, J., Luo, Y."Hemichannel‑mediated volume regulation contributes to IPC‑induced cardiomyocyte protection". Experimental and Therapeutic Medicine 17, no. 3 (2019): 1847-1854. https://doi.org/10.3892/etm.2018.7127