Abstract

Mesenchymal stem cells (MSCs) are adult stromal cells that reside in virtually all postnatal tissues. Due to their regenerative and immunomodulatory capacities, MSCs have attracted growing attention during the past two decades. MSC-derived extracellular vesicles (MSC-EVs) are able to duplicate the effects of their parental cells by transferring functional proteins and genetic materials to recipient cells without cell-to-cell contact. MSC-EVs also target macrophages, which play an essential role in innate immunity, adaptive immunity, and homeostasis. Recent studies have demonstrated that MSC-EVs reduce M1 polarization and/or promote M2 polarization in a variety of settings. In this review, we discuss the mechanisms of macrophage polarization and roles of MSC-EV-induced macrophage polarization in the outcomes of cardiovascular, pulmonary, digestive, renal, and central nervous system diseases. In conclusion, MSC-EVs may become a viable alternative to MSCs for the treatment of diseases in which inflammation and immunity play a critical role.

Highlights

  • Mesenchymal stem cells (MSCs) are present in a variety of tissue sources and possess multi-lineage differentiation potential

  • Mesenchymal stem (stromal) cells (MSCs)-Extracellular vesicles (EVs) exhibit the biological effects of their parental cells via transfer of functional components to target cells

  • MSC-derived extracellular vesicles (MSC-EVs) are capable of targeting macrophages in the tissue and inducing the polarization macrophage polarization from M1 to M2 phenotype

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Summary

Introduction

Mesenchymal stem (stromal) cells (MSCs) are present in a variety of tissue sources and possess multi-lineage differentiation potential. MSC-EVs alleviated myocardial ischemia/reperfusion injury via transfer of miR-182, which induced M2 macrophages polarization via targeting TLR4. MSC-EV-mediated macrophage polarization in cardiovascular diseases In a mouse elastase-induced model of abdominal aortic aneurysm, Spinosa et al reported that miR-147, a negative regulator of macrophage inflammatory responses, was significantly elevated compared with controls.

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