Topical JAG1, a Notch Activator, Accelerates Closure of Splinted Cutaneous Excisional Wounds in Wild-Type Mice
Kayla Leibl, BS, Alex Martin, undergraduate student, Timothy W. King, MD, PhD, FAAP, FACS.
University of Wisconsin, Madison, WI, USA.
Annually in the USA, >6.5M patients suffer from wound-related complications, and treatment cost is >$25B. We are interested in improving the wound healing process. We have previously shown that inhibition of Notch decreases wound healing. Therefore, in this experiment we hypothesize that activation of the Notch pathway, via JAG1, would accelerate the rate of wound healing in a splinted cutaneous excisional wound model.
8-week old, male mice (n=44) were anesthetized, shaved, and two 1cm2 full-thickness wounds were created on their backs under aseptic conditions. A 12-mm stent was secured around each wound to prevent healing by contraction. Sterile dressings were applied. Dressings were changed daily after topical application of JAG1 (10 nM) or vehicle (PBS) for 17 days. Digital photographs were taken daily. Wounds were analyzed using ImageJ. Wound closure was defined by visualization of resurfacing epithelia. Statistical significance was defined as p<0.05 using the students’ t-test.
Wound sizes were similar in both groups at the beginning of treatment. JAG1 significantly accelerated the rate of wound closure compared to control by day 11 (11.18±1.15 vs 7.59±1.13 respectively, p<0.03) and remained significantly accelerated throughout the experiment. Wound closure for the JAG1 group occurred on Day 17. The control group was not completely closed at Day 17.
JAG1, a Notch activator, accelerates cutaneous wound closure in vivo. Based on this novel finding, further studies should evaluate the mechanisms by which Notch accelerates wound healing. This could result in the development of new therapeutics for wound healing in patients.
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