Macrophages are heterogeneous multifunctional leukocytes which are regulated in a tissue- and disease-specific context. Many different studies have been published using in vitro macrophage models to study disease. Here, we aggregated public expression data to define consensus expression profiles for eight commonly-used in vitro macrophage models. Altogether, we observed well-known but also novel markers for different macrophage subtypes.
BACKGROUND AND AIMS: Atherosclerosis is a lipid-driven chronic inflammatory disorder of the arteries, and monocytes and macrophages play a central role in this process. Within the atherosclerotic lesion, macrophages can scavenge modified lipids and become the so-called foam cells. We previously reported that the epigenetic enzyme Kdm6b (also known as Jmjd3) controls the pro-fibrotic transcriptional profile of peritoneal foam cells.
The chronic remitting and relapsing intestinal inflammation characteristic of Crohn’s disease frequently leads to fibrosis and subsequent stenosis of the inflamed region. Approximately a third of all Crohn’s disease patients require resection at some stage in their disease course. As the pathogenesis of Crohn’s disease associated fibrosis is largely unknown, a strong necessity exists to better understand the pathophysiology thereof.
Macrophages are key immune cells found in atherosclerotic plaques and critically shape atherosclerotic disease development. The epigenomic enzyme Histone deacetylase 3 (HDAC3) has a role in regulating the atherosclerotic phenotype of macrophages. In rodents, myeloid HDAC3 deficiency promotes collagen deposition in atherosclerotic lesions and thus induces a stable plaque phenotype. Also, macrophages presented a switch to anti-inflammatory wound healing characteristics and showed improved lipid handling.