Macrophages and stem/progenitor cells interplay in adipose tissue and skeletal muscle: a review

Abstract

Like all immune cells, macrophages do not act autonomously but in unison with other immune cells, surrounding tissues, and the niche they occupy. Constant exchange of information between cellular and noncellular participants within a tissue allows for preserving homeostasis and defining responses in a pathologic environment. Although molecular mechanisms and pathways involved in reciprocal signaling between macrophages and other immune cells have been known for decades, much less is known about interactions between macrophages and stem/progenitor cells. Based on the time when stem cells form, there are two stem cell types: embryonic stem cells existing only in an early embryo, which are pluripotent and can differentiate into any cell type present in an adult, and somatic (adult) stem cells formed in fetus and persisting for whole adult life. Tissues and organs have their own (tissue-specific and organ-specific) adult stem cells, which serve as a reserve for tissue homeostasis and regeneration after injury. It is still uncertain whether organ-and tissue-specific stem cells are actual stem cells or just progenitor cells. The important question is how stem/progenitor cells can sculpt macrophage phenotype and functions. Even less is known if or how macrophages can shape stem/progenitor cell functions, their divisions, and fate. We describe here examples from recent studies of how stem/progenitor cells can affect macrophages and how macrophages can influence stem/progenitor cell properties, functions, and destiny.

History and future perspectives of adipose tissue macrophage biology

“…After birth, hematopoiesis switches from the fetal liver to the thymus and bone marrow, and the bone marrow becomes the primary source of all blood cell lines, including circulating monocytes ( Kloc et al, 2023 ). Macrophages, which are increased in adipose tissue during obesity, have also been reported to be induced in adipose tissue by bone marrow-derived monocytes in an MCP1/CCR2 pathway-dependent manner ( Kamei et al, 2006 ; Kanda et al, 2006 ; Weisberg et al, 2006 ; Lumeng et al, 2008 ) ( Figure 1B ).…”