| First Author | Hou C | Year | 2021 |
| Journal | Wound Repair Regen | Volume | 29 |
| Issue | 2 | Pages | 306-315 |
| PubMed ID | 33378794 | Mgi Jnum | J:341679 |
| Mgi Id | MGI:7541702 | Doi | 10.1111/wrr.12885 |
| Citation | Hou C, et al. (2021) Knockout of sodium channel Na(x) delays re-epithelializathion of splinted murine excisional wounds. Wound Repair Regen 29(2):306-315 |
| abstractText | Mammalian wound healing is a carefully orchestrated process in which many cellular and molecular effectors respond in concert to perturbed tissue homeostasis in order to close the wound and re-establish the skin barrier. The roles of many of these molecular effectors, however, are not entirely understood. Our lab previously demonstrated that the atypical sodium channel Na(x) (encoded by Scn7a) responds to wound-induced epidermal dehydration, resulting in molecular cascades that drive pro-inflammatory signaling. Acute inhibition of Na(x) was sufficient to attenuate dermatopathological symptoms in models of hypertrophic scar and dermatitis. To date, however, the role of Na(x) in excisional wound healing has not been demonstrated. Here we report development of a knockout mouse that lacks expression of functional Na(x) , and we demonstrate that lack of functional Na(x) results in deficient wound healing in a murine splinted excisional wound healing model. This deficiency in wound healing was reflected in impaired re-epithelialization and decreased keratinocyte proliferation, a finding which was further supported by decreased proliferation upon Na(x) knockdown in HaCaT cells in vitro. Defective wound healing was observed alongside increased expression of inflammatory genes in the wound epidermis of Na(x) (-/-) mice, suggesting that mice lacking functional Na(x) retain the ability to undergo skin inflammation. Our observations here motivate further investigation into the roles of Na(x) in wound healing and other skin processes. |
