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Updated: Apr 12, 2026
Characterizing Epithelial Wound Healing In Vivo Using the Cnidarian Model Organism Clytia hemisphaerica
Published on: February 10, 2023
Connexin43 plays diverse roles in co-ordinating cell migration and wound closure events
Claire Lorraine1, Catherine S Wright1, Patricia E Martin1
1*Department of Life Sciences and Institute for Applied Health Research, Glasgow Caledonian University, Glasgow G4 0BA, U.K.
Abstract:
Chronic wounds are not only debilitating to patients, but also impose a huge financial burden on healthcare providers, as current treatments are not particularly effective. Wound healing is a highly co-ordinated process involving a vast array of signalling molecules and different cell types, therefore a substantial amount of research has been carried out in the quest to develop new therapies. The gap junction (GJ) protein connexin43 (Cx43) is one of the many molecules whose expression has been found to be up-regulated in chronic wounds and as a result targeting it may have therapeutic potential. Two different approaches have been adopted to investigate this: knockdown of Cx43 using antisense oligonucleotides and connexin mimetic peptides (CMPs) which inhibit the function of Cx43 without affecting gene expression. These peptides are targeted to the C-terminal domain or the extracellular loops of Cx43 and thus are likely to function by different means. However, both block channel function and have been shown to enhance cell migration rates. In recent years, non-channel functions have emerged for Cx43, many of which are linked to cytoskeletal dynamics and the extracellular matrix (ECM), showing that Cx43 plays diverse roles in co-ordinating wound closure events. It is clear that both CMPs and antisense oligonucleotides hold therapeutic potential, however maintaining Cx43 expression may be beneficial to the cell by preserving other non-channel functions of Cx43. Recent data in the field will be discussed in this article.
Insights
Targeting connexin43 (Cx43) shows therapeutic potential for chronic wounds. Inhibiting Cx43 enhances cell migration, but preserving its expression may maintain beneficial non-channel functions for wound healing.
Area of Science:
- Cell biology
- Wound healing research
- Biomedical engineering
Background:
- Chronic wounds present significant patient and economic challenges due to ineffective treatments.
- Wound healing is a complex biological process involving intricate signaling pathways and cellular interactions.
- Connexin43 (Cx43) expression is elevated in chronic wounds, suggesting its potential as a therapeutic target.
Purpose of the Study:
- To explore the therapeutic potential of targeting connexin43 (Cx43) in chronic wound healing.
- To investigate the effects of Cx43 modulation on cell migration and other wound closure mechanisms.
- To differentiate the impact of blocking Cx43 channel function versus preserving its non-channel roles.
Main Methods:
- Utilizing antisense oligonucleotides to reduce Cx43 gene expression (knockdown).
- Employing connexin mimetic peptides (CMPs) to inhibit Cx43 channel function without altering gene expression.
- Analyzing the effects of these interventions on cell migration rates and cytoskeletal dynamics.
Main Results:
- Both antisense oligonucleotides and CMPs targeting Cx43 enhance cell migration rates.
- Cx43 exhibits diverse non-channel functions, including roles in cytoskeletal dynamics and extracellular matrix interaction.
- Inhibition of Cx43 channel function is demonstrated, with potential for different mechanisms based on peptide targeting.
Conclusions:
- Modulating Cx43 offers promising therapeutic avenues for chronic wound treatment.
- While inhibiting Cx43 can accelerate cell migration, maintaining its expression may preserve crucial non-channel functions.
- Further research is needed to balance the benefits of Cx43 inhibition with the preservation of its essential cellular roles in wound repair.
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