ArticleExperimental and therapeutic medicine2019
Hemichannel-mediated volume regulation contributes to IPC-induced cardiomyocyte protection.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Channel Behavior and Voltage Gating of a Cx43 Mutant Simulating Preconditioning.Bioelectricity · 2023Article
- Imaging in experimental models of diabetes.Acta diabetologica · 2022Review
- Cardiac Connexin-43 Hemichannels and Pannexin1 Channels: Provocative Antiarrhythmic Targets.International journal of molecular sciences · 2020Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 µm
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