LpL deficiency altered macrophage gene expression and reduced lipid uptake in vitro, but these phenotypic changes were not mimicked in tissue macrophages in vivo.
In vitro phenotypic changes in macrophages caused by LpL deletion are not replicated in tissue macrophages in vivo, suggesting different mechanisms govern in vivo macrophage polarization.
Objective: Fatty acid uptake and oxidation characterize the metabolism of alternatively activated macrophage polarization in vitro, but the in vivo biology is less clear. We assessed the roles of LpL (lipoprotein lipase)-mediated lipid uptake in macrophage polarization in vitro and in several important tissues in vivo. Approach and Results: We created mice with both global and myeloid-cell specific LpL deficiency. LpL deficiency in the presence of VLDL (very low-density lipoproteins) altered gene expression of bone marrow–derived macrophages and led to reduced lipid uptake but an increase in some anti- and some proinflammatory markers. However, LpL deficiency did not alter lipid accumulation or gene expression in circulating monocytes nor did it change the ratio of Ly6C high /Ly6C low . In adipose tissue, less macrophage lipid accumulation was found with global but not myeloid-specific LpL deficiency. Neither deletion affected the expression of inflammatory genes. Global LpL deficiency also reduced the numbers of elicited peritoneal macrophages. Finally, we assessed gene expression in macrophages from atherosclerotic lesions during regression; LpL deficiency did not affect the polarity of plaque macrophages. Conclusions: The phenotypic changes observed in macrophages upon deletion of Lpl in vitro is not mimicked in tissue macrophages.
Chang et al. (Thu,) conducted a other in Macrophage polarization. LpL (lipoprotein lipase) deficiency vs. Control was evaluated on Macrophage polarization and lipid uptake. LpL deficiency altered macrophage gene expression and reduced lipid uptake in vitro, but these phenotypic changes were not mimicked in tissue macrophages in vivo.