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Elevated Kallikrein-binding protein in diabetes impairs wound healing through inducing macrophage M1 polarization.

Cell Commun. Signal. 2019-06; 
FengJuan,DongChang,LongYanlan,MaiLifang,RenMeng,LiLingyi,ZhouTi,YangZhonghan,MaJianxing,YanLi,YangXia,GaoGuoquan,QiWe
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Catalog Antibody IgG (Sigma-Aldrich, St. Louis, MO, USA) or KBP-neutralizing antibody (Genscript, China) was intraperitoneally administered to the diabetic mice every day beginning three days before the establishment of a wound model for 15 days. Get A Quote

摘要

The accumulation of M1-polarized macrophages and excessive inflammation are important in the pathogenesis of diabetic foot ulcer (DFU). However, the underlying mechanism of DFU pathogenesis and the crucial regulators of DFU are less well known. Our previous study reported that kallikrein-binding protein (KBP), an angiogenesis inhibitor, was significantly upregulated in diabetic patients compared to its levels in controls. The effects of KBP on monocyte chemotaxis and macrophage M1 polarization were elucidated in this study.

关键词

Diabetic wound healing,Kallikrein-binding protein,Monocyte-macrophages,Notch/NF-κB signal
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