GSE195727
Placental dysfunction influences fetal monocyte subpopulation gene expression in preterm birth
Purpose: Identify differences in gene expression profiles in fetal monocytes - cells that persist and differentiate postnatally -  according to distinct placental histologic domains. Methods: We first isolated classical and intermediate monocyte  subsets via FACS and performed transcriptomic profiling of 140 samples (70 classical and 70  intermediate monocyte samples) using bulk RNA-Seq. Results: We report that placental lesions are associated with gene expression changes in fetal  monocyte subsets. Specifically,fetal monocytes exposed to acute placental  inflammation upregulate biological processes related to monocyte activation, monocyte  chemotaxis, and platelet function while monocytes exposed to maternal vascular malperfusion  lesions downregulate these processes. Additionally, we show that intermediate monocytes might  be a source of mitogens, such as HBEGF, NRG1, and VEGFA, implicated in different outcomes  related to prematurity. Conclusions: This is the first study to show that placental lesions are associated with  unique changes in fetal monocytes and monocyte subsets. As fetal monocytes persist and  differentiate into various phagocytic cells following birth, our study may provide insight into  morbidity related to prematurity and ultimately potential therapeutic targets. Overall design: Gene expression profiles of sorted fetal monoctyes.