Liu Zhongyang, Xu Yingbin, Chen Lei, Xie Julin, Tang Jinming, Zhao Jingling, Shu Bin, Qi Shaohai, Chen Jian, Liang Guangping, Luo Gaoxing, Wu Jun, He Weifeng, Liu Xusheng
Department of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou, 510080, Guangdong, P. R. China.
State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, P. R. China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, P. R. China.
Am J Transl Res. 2016 May 15;8(5):2375-84. eCollection 2016.
The impairment of skin repair in diabetic patients can lead to increased morbidity and mortality. Proper proliferation, apoptosis and migration in keratinocytes are vital for skin repair, but in diabetic patients, hyperglycemia impairs this process. Dendritic epidermal T cells (DETCs) are an important part of the resident cutaneous immunosurveillance program. We observed a reduction in the number of DETCs in a streptozotocin-induced diabetic mouse model. This reduction in DETCs resulted in decreased IGF-1 and KGF production in the epidermis, which is closely associated with diabetic delayed wound closure. DETCs ameliorated the poor wound-healing conditions in diabetic mice by increasing keratinocyte migration and proliferation and decreasing keratinocyte apoptosis in diabetes-like microenvironments. Our results elucidate a new mechanism for diabetic delayed wound closure and point to a new strategy for the treatment of wounds in diabetic patients.
糖尿病患者皮肤修复功能受损会导致发病率和死亡率增加。角质形成细胞的正常增殖、凋亡和迁移对皮肤修复至关重要，但在糖尿病患者中，高血糖会损害这一过程。树突状表皮T细胞（DETCs）是皮肤常驻免疫监视程序的重要组成部分。我们在链脲佐菌素诱导的糖尿病小鼠模型中观察到DETCs数量减少。DETCs数量的减少导致表皮中IGF-1和KGF生成减少，这与糖尿病伤口愈合延迟密切相关。在类似糖尿病的微环境中，DETCs通过增加角质形成细胞迁移和增殖以及减少角质形成细胞凋亡，改善了糖尿病小鼠伤口愈合不良的状况。我们的研究结果阐明了糖尿病伤口愈合延迟的新机制，并为糖尿病患者伤口治疗指出了新策略。
