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

ABSTRACT:

Background

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.

Methods

Plasma KBP levels and monocyte counts were assessed by ELISA and flow cytometry. Wound closure rates in different groups were monitored daily. The phenotype and recruitment of macrophages were measured by real-time PCR, western blot and

SUBMITTER: Feng J 

PROVIDER: S-EPMC6558923 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature