Project description:We report that obese fat tissue of mice contain multiple distinct populations of adipose tissue macrophage (ATM) with unique transcriptomes and chromatin landscapes. Mouse Ly6c ATMs express genes that are adipogenic, while CD9 ATMs express pro-inflammatory genes under the control of activating transcription factors. Adoptive transfer of Ly6c ATMs into lean mice activates gene programs typical of normal adipocyte physiology. By contrast, adoptive transfer of CD9 ATMs drives gene expression that is characteristic of obesity.
Project description:We report that obese fat tissue of mice contain multiple distinct populations of adipose tissue macrophage (ATM) with unique transcriptomes and chromatin landscapes. Mouse Ly6c ATMs express genes that are adipogenic, while CD9 ATMs express pro-inflammatory genes under the control of activating transcription factors. Adoptive transfer of Ly6c ATMs into lean mice activates gene programs typical of normal adipocyte physiology. By contrast, adoptive transfer of CD9 ATMs drives gene expression that is characteristic of obesity.
Project description:We report that obese fat tissue of mice contain multiple distinct populations of adipose tissue macrophage (ATM) with unique transcriptomes and chromatin landscapes. Mouse Ly6c ATMs express genes that are adipogenic, while CD9 ATMs express pro-inflammatory genes under the control of activating transcription factors. Adoptive transfer of Ly6c ATMs into lean mice activates gene programs typical of normal adipocyte physiology. By contrast, adoptive transfer of CD9 ATMs drives gene expression that is characteristic of obesity.
Project description:The objective of this study was to characterise macrophage subsets in bone marrow (BM) isolated from Csf1r-EGFP mice. A concurrent imaging flow cytometry study conducted by our team unexpectedly revealed macrophage surface marker staining emanates from membrane-bound subcellular remnants associated with unrelated cells. Expression data from sorted BM “macrophage” populations was found to be consistent with macrophage fragments associated with non-macrophage cells. Granulocyte-specific genes were enriched within the CD11b+ “macrophage” (CD11b+F4/80+Ly6G-GFPloVCAM1+) populations, whereas CD11b- “macrophages” (CD11b-F4/80+GFP+VCAM1+) were consistent with a mixed cell population including both plasma cells and erythroblasts. This data demonstrates how fragmentation of hematopoietic tissue macrophages can result in misattribution of macrophage identity to non-macrophage populations, thereby undermining accuracy of macrophage ex vivo molecular profiles.