Abstract
Delayed repair is a serious public health concern for diabetic populations. Intercellular adhesion molecule 1 (ICAM-1) and Lymphocyte function-associated antigen 1 (LFA-1) play important roles in orchestrating the repair process. However, little is known about their effects on endothelial cell (EC) proliferation and neutrophil activity in subjects with hyperglycemia (HG). We cultured ECs and performed a scratch-closure assay to determine the relationship between ICAM-1 and EC proliferation. Specific internally labeled bacteria were used to clarify the effects of ICAM-1 and LFA-1 on neutrophil phagocytosis. Transwell assay and fluorescence-activated cell sorting analysis evaluated the roles of ICAM-1 and LFA-1 in neutrophil recruitment. ICAM-1+/+ and ICAM-1–/– mice were used to confirm the findings in vivo. The results demonstrated that HG decreased the expression of ICAM-1, which lead to the low proliferation of ECs. HG also attenuated neutrophil recruitment and phagocytosis by reducing the expression of ICAM-1 and LFA-1, which were strongly associated with the delayed repair.
Highlights
Diabetes mellitus is a chronic metabolic disorder characterized by inappropriate hyperglycemia (HG) (American Diabetes, 2013)
As Lymphocyte function-associated antigen 1 (LFA-1) expression was implicated in neutrophil phagocytic activity, we explored the effects of LFA-1 on neutrophil phagocytosis in Intercellular adhesion molecule 1 (ICAM-1)+/+-HG injury tissue
The scratch-closure assays of NG and HG cultured tissues demonstrated that HG decreases ICAM-1 expression, which results in low endothelial cell (EC) proliferation
Summary
Diabetes mellitus is a chronic metabolic disorder characterized by inappropriate hyperglycemia (HG) (American Diabetes, 2013). Uncontrolled HG can lead to a host of diabetic complications, including delayed injury repair, which is a serious public health concern for subjects with diabetes. The tendon injury repair process consists of four phases: coagulation, inflammation, granular tissue formation, and remodeling (Gosain and DiPietro, 2004; Falanga, 2005). All the phases rely strongly on cellular and metabolic components of the inflamed microenvironment. The diabetic injury microenvironment is hostile and characterized by markedly elevated levels of inflammatory cytokines, which contribute to the dysfunction of these components. ICAM-1 regulates EC permeability in inflamed tissues by inducing the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) (Han et al, 2016). Due to the complexity of the immune response under HG conditions, the potential effects
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