Abstract
During wound healing and reconstruction, epidermal stem cells (ESCs) migrate to the wound site and activate to repair the damaged epithelium. Moreover, there exist complicate signaling pathways to regulate wound regeneration including Notch signaling. The Notch signaling pathway is a regulator of epidermal differentiation, which may be an important mediator of wound regeneration that participates in various processes, from the development of the dermis to the formation of skin appendages. Here, we show that Notch signaling pathways are upregulated by Jagged1 in ESCs and stem cell characteristics of ESCs change when Notch1 signaling varies. By administration of siRNAJagged1 knockdown ESCs in wounds, we observe that the suppression of Jagged1 down regulate expression of Notch signaling and resulted in poor-quality wound healing. Connecting Notch1 pathways activity to ESCs response to wound repairing may develop a new therapeutic strategy for delayed healing.
Highlights
The skin is the largest organ in the human body and functions as a barrier from environmental aggressions, such as external microorganisms or dehydration
Notch1 signaling pathway is activated in response to wounding and there exist some relationship between Notch1 and epidermal stem cells (ESCs) during wound repairing
These results implied that Notch1 signaling pathway was involved in wound repairing which induced by ESCs
Summary
The skin is the largest organ in the human body and functions as a barrier from environmental aggressions, such as external microorganisms or dehydration. The mechanism of signaling pathways related to ESC proliferation and differentiation should be explored because these actions may improve the speed and quality of wound healing and promote the structure and function of physiological repair. Recent evidence has suggested that Notch signaling plays a pivotal role in wound repairing, including accelerated wound closure, pro-migratory effects of fibroblast and vascular endothelial cells, increased collagen deposition and vascularity, and that it is required for proper healing [12,13,14]. Notch is well known as a regulator of epidermal differentiation of skin [9,15,16], but its role in this process during the re-epithelialization of healing wounds is relatively unexplored. Elucidating the molecular mechanisms controlling the behavior of ESCs will provide novel strategies for the treatment of chronic wound
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