Abstract
The human response to serious cutaneous damage is limited to relatively primitive wound healing, whereby collagenous scar tissue fills the wound bed. Scars assure structural integrity at the expense of functional regeneration. In contrast, axolotls have the remarkable capacity to functionally regenerate full thickness wounds. Here, we identified a novel role for SALL4 in regulating collagen transcription after injury that is essential for perfect skin regeneration in axolotl. Furthermore, we identify miR-219 as a molecular regulator of Sall4 during wound healing. Taken together, our work highlights one molecular mechanism that allows for efficient cutaneous wound healing in the axolotl.
Highlights
The skin is the largest organ of the human body and has several crucial functions to keep the body operational and healthy
SALL4 was expressed at high levels in many dermal cells in the axolotl skin during wound healing (Figures 1 and 2; Supplementary Figure 2), we focused on SALL4
In this study, we have identified a novel role for the transcription factor SALL4 in regulating collagen expression and deposition during scar-free wound healing in axolotl
Summary
The skin is the largest organ of the human body and has several crucial functions to keep the body operational and healthy. Humans can repair minor tears to the skin but major skin injuries result in incompletely remodelled collagen in the wound bed, which manifests as part of a fibrotic scar.[1,2,3,4,5,6]. The Mexican ‘Axolotl’ salamander is able to fully regenerate the skin after major wounding.[7,8,9,10] Previous work shows that at the end of the wound healing process in axolotls collagen remodelling and wound bed closure is complete, and the skin is restored to normal functionality. A common hypothesis is that axolotl and human have differing molecular mechanisms of cutaneous wound healing that directs towards scar-free regeneration in axolotls versus reparative scar prone healing in humans
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