Abstract：
Aim: This study aimed to explore the role of EGFL7 in the healing process of refractory diabetic wounds. Methods: Epidermal stem cells (ESCs) were isolated from healthy mice and diabetic mice, identified by immunofluorescence, transfected with EGFL7 overexpression and silencing lentiviral vectors, and treated with Notch pathway inhibitor (DAPT). Results: SiEGFL7 significantly inhibited the proliferation, invasion and migration of ESCs of healthy mice. DAPT prominently inhibited the expressions of Notch1, Notch2, Hes1 and Jag1 in ESCs of healthy mice induced by overexpressed EGFL7. Overexpressed EGFL7 promoted wound healing in diabetic mice with refractory wounds. Conclusion: EGFL7 affects the proliferation and migration of ESCs in refractory diabetic wounds by regulating the Notch signaling pathway.
EGFL7 silencing inhibited the proliferation, invasion and migration of ESCs of healthy mice, which was reversed by Notch signaling inhibition. Overexpressed EGFL7 promoted wound healing in diabetic mice with refractory wounds, providing a promising potential for the treatment of diabetic wound.
EGFL7 silencing inhibited the proliferation, invasion and migration of ESCs of healthy mice, which was reversed by Notch signaling inhibition. Overexpressed EGFL7 promoted wound healing in diabetic mice with refractory wounds, providing a promising potential for the treatment of diabetic wound.
摘要：
目的:探讨EGFL7在难治性糖尿病创面愈合过程中的作用。方法:从健康小鼠和糖尿病小鼠中分离表皮干细胞(ESCs),通过免疫荧光鉴定，用EGFL7过表达和沉默慢病毒载体转染，并用Notch通路抑制剂(DAPT)处理。结果:SiEGFL7能显著抑制细胞增殖,健康小鼠ESCs的侵袭和迁移。DAPT显著抑制过表达EGFL7诱导的健康小鼠ESCs中Notch1、Notch2、Hes1和Jag1的表达。在具有难治性伤口的糖尿病小鼠中,过表达的EGFL7促进伤口愈合。结论:EGFL7通过调节Notch信号通路影响糖尿病难愈性创面ESCs的增殖和迁移。
EGFL7沉默抑制增殖，健康小鼠ESCs的侵袭和迁移，这被Notch信号抑制所逆转。过表达EGFL7促进糖尿病小鼠难治性伤口的伤口愈合，为糖尿病伤口的治疗提供了有希望的潜力。
EGFL7沉默抑制增殖，健康小鼠ESCs的侵袭和迁移，这被Notch信号抑制所逆转。过表达EGFL7促进糖尿病小鼠难治性伤口的伤口愈合，为糖尿病伤口的治疗提供了有希望的潜力。
