Abstract
Mesenchymal stem cells (MSCs) are multipotent adult stromal cells widely studied for their regenerative and immunomodulatory properties. They are capable of modulating macrophage plasticity depending on various microenvironmental signals. Current studies have shown that metabolic changes can also affect macrophage fate and function. Indeed, changes in the environment prompt phenotype change. Therefore, in this review, we will discuss how MSCs orchestrate macrophage’s metabolic plasticity and the impact on their function. An improved understanding of the crosstalk between macrophages and MSCs will improve our knowledge of MSC’s therapeutic potential in the context of inflammatory diseases, cancer, and tissue repair processes in which macrophages are pivotal.
Highlights
Mesenchymal stem/stromal cells (MSCs) are multipotent cells with the capacity of differentiating into cells from the mesodermal tissue such as adipocytes, chondrocytes, and osteoblasts cells [1, 2]
In this review, we synthesize macrophage response evidence driven by mesenchymal stem cell-mediated metabolic reprogramming and how this regulation will impact the progression of several inflammatory and autoimmune diseases
It has been reported that STAT3 deletion causes a reduction in the activity of complexes I and II [149]. These results suggest that Mesenchymal stem cells (MSCs) could be favoring an oxidative phosphorylation (OXPHOS) metabolism in macrophage and, in turn, inducing M2 polarization through TNF-stimulated gene 6 (TSG-6) secretion
Summary
Mesenchymal stem/stromal cells (MSCs) are multipotent cells with the capacity of differentiating into cells from the mesodermal tissue such as adipocytes, chondrocytes, and osteoblasts cells [1, 2]. MSCs promote an enhanced FAO metabolic status and inhibition of the glycolytic metabolism in macrophage, features of anti-inflammatory M2 macrophage in detrimental pro-inflammatory M1 macrophage, respectively (Figure 2) These metabolic reprogramming processes are driven by MSCs through the tight regulation of molecules such as AMPK, mTOR, Sirtuin, either at the mRNA or protein levels. The repolarization of TAMs into M1-like macrophage has successfully produced antitumoral responses in preclinical murine models [130] In this context, MSCs have been shown to promote tumor progression by inhibiting the release of pro-inflammatory cytokines and increasing the generation of M2-like macrophage through the secretion of a variety of immunomodulatory molecules such as PGE2, IL1RA, TGF-b, and IL-8 [32, 131]. Regarding what we have described in this review on the MSC/ macrophage dialogue, modified MSC could communicate with macrophage to switch their metabolism and their inflammatory status by directing them towards a proregenerative phenotype and indirectly promoting regeneration
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