Antimicrobial peptide derived from insulin‐like growth factor‐binding protein 5 improves diabetic wound healing
-
- Hainan Yue
- Department of Dermatology and Allergology University Graduate School of Medicine Tokyo Japan
-
- Pu Song
- Department of Dermatology, Xijing Hospital Fourth Military Medical University Xi'an, Shannxi China
-
- Nutda Sutthammikorn
- Department of Microbiology, Faculty of Medicine Chiang Mai University Chiang Mai Thailand
-
- Yoshie Umehara
- Atopy (Allergy) Research Center Juntendo University Graduate School of Medicine Tokyo Japan
-
- Juan Valentin Trujillo‐Paez
- Atopy (Allergy) Research Center Juntendo University Graduate School of Medicine Tokyo Japan
-
- Hai Le Thanh Nguyen
- Department of Dermatology and Allergology University Graduate School of Medicine Tokyo Japan
-
- Miho Takahashi
- Department of Dermatology and Allergology University Graduate School of Medicine Tokyo Japan
-
- Ge Peng
- Department of Dermatology and Allergology University Graduate School of Medicine Tokyo Japan
-
- Risa Ikutama
- Department of Dermatology and Allergology University Graduate School of Medicine Tokyo Japan
-
- Ko Okumura
- Atopy (Allergy) Research Center Juntendo University Graduate School of Medicine Tokyo Japan
-
- Hideoki Ogawa
- Atopy (Allergy) Research Center Juntendo University Graduate School of Medicine Tokyo Japan
-
- Shigaku Ikeda
- Department of Dermatology and Allergology University Graduate School of Medicine Tokyo Japan
-
- François Niyonsaba
- Atopy (Allergy) Research Center Juntendo University Graduate School of Medicine Tokyo Japan
説明
<jats:title>Abstract</jats:title><jats:p>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.</jats:p>
収録刊行物
-
- Wound Repair and Regeneration
-
Wound Repair and Regeneration 30 (2), 232-244, 2022-02-05
Wiley
