We performed RNA-seq on tissue biopsies derived from patients with DFUs and compared it to human oral and skin wounds to identify the molecular mechanisms and transcriptional networks that are deregulated in DFUs. Our results identified a unique inflammatory transcriptional signature unique to oral and skin wounds involved in promoting cell proliferation and cell survival of immune cells that are deficient in DFUs. In addition, we identified a signature immune-cell profile in which activation and proliferation of macrophages and neutrophils were absent in DFUs. These results suggest that a deregulated immune response in which impaired activation, proliferation and survival of immune cells contribute to pathogenesis of DFUs and provides novel avenues for development of therapies aimed at reprogramming DFUs into healing-competent wounds. SOURCE: Stephen,R,Brooks (stephen.brooks@nih.gov) -  NIAMS/NIH

Pluto Bioinformatics

GSE134431: Deregulated immune signature orchestrated by FOXM1 impairs human diabetic wound healing