Neutrophils are involved in the first stage of acute
inflammation. After injury, they are mobilized and recruited to the injured tissue. In diabetes, wound healing is delayed and aberrant, leading to excessive recruitment and retention of neutrophils that fail to promote angiogenesis and prolong
inflammation. However, the exact pathological mechanisms of diabetic-derived neutrophils in chronic
inflammation remain unclear. Here,
miRNA profiling of neutrophils from bone marrow in type 2 diabetic mice was performed using a microarray.
miRNAs regulate the posttranscriptional expression of target mRNAs and are important in countering
inflammation-related diseases. Our study revealed that
miRNAs exhibit differential expression in diabetic-derived neutrophils compared with non-diabetic-derived neutrophils, especially miR-129 family members. miR-129-2-3p directly regulated the translation of Casp6 and Ccr2, which are involved in inflammatory responses and apoptosis. Furthermore, miR-129-2-3p overexpression at the
wound site of type 2 diabetic mice accelerated wound healing. These results suggest possible involvement of miR-129-2-3p in diabetic-derived neutrophil dysfunction and that retention kinetics of neutrophils and chronic
inflammation may be initiated through miR-129-2-3p-regulated genes. This study characterizes changes in global
miRNA expression in diabetic-derived neutrophils and systematically identifies critical target genes involved in certain biological processes related to the pathology of diabetic wound healing.