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Enhanced Wound Healing By Treatment with Heat Stable Antigen (HSA/CD24)

Background: Healthy individuals rarely have problems with wound healing. Most skin lesions heal rapidly and efficiently within one to two weeks. However, many medical and surgical complications can be attributed to deficiencies in wound repair. Open wounds have lost the barrier that protects tissues from bacterial invasion and allows the escape of vital fluids. Without expeditious healing, infections become more frequent. The CD24 gene encodes a heavily-glycosylated cell surface protein anchored to the membrane by phosphatidylinositol. CD24 plays an important role in the adaptive immune response and controls an important genetic checkpoint for homeostasis and autoimmune diseases in both mice and humans. We have previously shown that over expression of CD24results in increased proliferation and migration rates, and that its deficiency leads to impaired wound healing.

Aim: to examine the use of CD24 in enhancing the wound healing process.

Methods: An incisional model of wound healing was used and wound healing was studied in wild-type (WT) mice treated by subcutaneous injections of CD24 derivatives from bacterial and mammalian cell sources. Results - 4 cm long full-thickness skin wounds were incised on the back of mice. The mice were locally treated by subcutaneous injections of CD24 derivatives from either bacterial or mammalian cell sources and compared to untreated mice. Wounds were histologically analyzed and scored, based on the degree of cellular invasion, granulation tissue formation, vascularity, and re-epithelialization. In the treated mice the wounds closed significantly faster then the untreated mice. No statistically significant difference was seen between bacterial and mammalian origin derivatives.

Conclusion Increased levels of CD24, even in the normal state, may be used to enhance wound repair.

Reference Citations: Shapira, Shiran et al. "Delayed Wound Healing in Heat Stable Antigen (HSA/CD24)-Deficient Mice." Ed. Ajay Goel. PLoS ONE 10.10 (2015): e0139787. PMC. Web. 2 Feb. 2017.