Functional Role of Non-Muscle Myosin II in Microglia: An Updated Review

Myosins are a remarkable superfamily of actin-based motor proteins that use the energy derived from ATP hydrolysis to translocate actin filaments and to produce force. Myosins are abundant in different types of tissues and involved in a large variety of cellular functions. Several classes of the myosin superfamily are expressed in the nervous system; among them, non-muscle myosin II (NM II) is expressed in both neurons and non-neuronal brain cells, such as astrocytes, oligodendrocytes, endothelial cells, and microglia. In the nervous system, NM II modulates a variety of functions, such as vesicle transport, phagocytosis, cell migration, cell adhesion and morphology, secretion, transcription, and cytokinesis, as well as playing key roles during brain development, inflammation, repair, and myelination functions. In this review, we will provide a brief overview of recent emerging roles of NM II in resting and activated microglia cells, the principal regulators of immune processes in the central nervous system (CNS) in both physiological and pathological conditions. When stimulated, microglial cells react and produce a number of mediators, such as pro-inflammatory cytokines, free radicals, and nitric oxide, that enhance inflammation and contribute to neurodegenerative diseases. Inhibition of NM II could be a new therapeutic target to treat or to prevent CNS diseases.

Automated summary

Myosins are a superfamily of actin-based motor proteins that play important roles in various cellular functions, with non-muscle myosin II (NM II) being expressed in neurons and non-neuronal brain cells. In the nervous system, NM II modulates functions such as vesicle transport, phagocytosis, cell migration, and inflammation, and inhibition of NM II could be a potential therapeutic target for CNS diseases. Microglia cells, as the principal regulators of immune processes in the CNS, react to stimuli and produce mediators that contribute to neurodegenerative diseases.