Genome-wide chromatin profiling using ATAC-seq of diabetic or non-diabetic murine haematopoietic stem cells (HSC)

To understand the underlying mechanisms and predict transcription factors implicated in the generation and sustained pro-inflammatory memory within HSCs, ATAC-seq was performed on bone marrow HSCs isolated from either diabetic or non-diabetic control mice. Differential peak analyses indicated that cells form diabetic mice had an altered chromatin structure, and pathway analysis of these differential sites revealed pathways associated with inflammation. Peak motif enrichment analysis implicated Runt-related transcription factor 1 (RUNX1), among others, to be significantly enriched. 4 diabetic mice samples and 4 non-diabetic control mice samples were used. Each sample was split in half, one half submitted as a baseline, unstimulated control and the other was stimulated with IL-1β.