伤口愈合
血管生成
生长因子
表皮生长因子
角质形成细胞生长因子
血管内皮生长因子
角质形成细胞
血管生长素
细胞生长
细胞生物学
STAT蛋白
成纤维细胞
癌症研究
医学
成纤维细胞生长因子
抗菌肽
碱性成纤维细胞生长因子
化学
药理学
血管内皮生长因子A
新生血管
抗菌剂
生物
细胞迁移
信号转导
炎症
类胡萝卜素
内皮干细胞
生长抑制
免疫学
作者
Hainan Yue,Pu Song,Nutda Sutthammikorn,Yoshie Umehara,Juan Valentín Trujillo-Páez,Hai Le Thanh Nguyen,Miho Takahashi,Ge Peng,Risa Ikutama,Ko Okumura,Hideoki Ogawa,Shigaku Ikeda,François Niyonsaba
摘要
Abstract Impaired keratinocyte functions are major factors that are responsible for delayed diabetic wound healing. In addition to its antimicrobial activity, the antimicrobial peptide derived from insulin‐like growth factor‐binding protein 5 (AMP‐IBP5) activates mast cells and promotes keratinocyte and fibroblast proliferation and migration. However, its effects on diabetic wound healing remain unclear. Human keratinocytes were cultured in normal or high glucose milieus. The production of angiogenic growth factor and cell proliferation and migration were evaluated. Wounds in normal and streptozotocin‐induced diabetic mice were monitored and histologically examined. We found that AMP‐IBP5 rescued the high glucose‐induced attenuation of proliferation and migration as well as the production of angiogenin and vascular endothelial growth factors in keratinocytes. The AMP‐IBP5‐induced activity was mediated by the epidermal growth factor receptor, signal transducer and activator of transcription 1 and 3, and mitogen‐activated protein kinase pathways, as indicated by the inhibitory effects of pathway‐specific inhibitors. In vivo, AMP‐IBP5 markedly accelerated wound healing, increased the expression of angiogenic factors and promoted vessel formation in both normal and diabetic mice. Overall, the finding that AMP‐IBP5 accelerated diabetic wound healing by protecting against glucotoxicity and promoting angiogenesis suggests that AMP‐IBP5 might be a potential therapeutic target for treating chronic diabetic wounds.
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