AI Article Synopsis
- * PKCμ, a specific protein kinase, plays an important role in wound healing by inhibiting intercellular communication and promoting the movement of skin cells, but the detailed mechanism behind this effect has not been fully understood until now.
- * The study shows that PKCμ directly interacts with Cx43, phosphorylating it at a specific site (S368), leading to its internalization and reduced function, thereby enhancing cell migration and facilitating wound healing in skin cells.
Article Abstract
Downregulation of intercellular communication through suppression of gap junctional conductance is necessary during wound healing. Connexin 43 (Cx43), a prominent gap junction protein in skin, is downregulated following wounding to restrict communication between keratinocytes. Previous studies found that PKCμ, a novel PKC isozyme, regulates efficient cutaneous wound healing. However, the molecular mechanism by which PKCμ regulates wound healing remains unknown. We have identified that PKCμ suppresses intercellular communication and enhances cell migration in an wound healing model by regulating Cx43 containing gap junctions. PKCμ can directly interact with and phosphorylate Cx43 at S368, which leads to Cx43 internalization and downregulation. Finally, utilizing phosphomimetic and non-phosphorylatable S368 substitutions and gap junction inhibitors, we confirmed that PKCμ regulates intercellular communication and wound healing by controlling Cx43-S368 phosphorylation. These results define PKCμ as a critical regulator of Cx43 phosphorylation to control cell migration and wound healing in keratinocytes.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10875573 | PMC |
| http://dx.doi.org/10.1016/j.isci.2024.109033 | DOI Listing |
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