TY - JOUR
T1 - The role of Galectin-3/MAC-2 in the activation of the innate-immune function of phagocytosis in microglia in injury and disease
AU - Rotshenker, Shlomo
PY - 2009/9
Y1 - 2009/9
N2 - Microglia are a self-sustained population of immune/myeloid cells present throughout the central nervous system (CNS). Microglia are in a "resting" state in the normal adult CNS. They turn "active" in injury and disease (e.g., trauma, neurodegeneration, and infection). Activated microglia can be beneficial as well as detrimental/neurotoxic. The innate-immune function of phagocytosis of tissue debris, neurotoxic factor, and pathogens is a beneficial function of microglia. The current manuscript reviews the role of Galectin-3 (known also as MAC-2; Galectin-3/MAC-2) in the activation of the phagocytosis of degenerated myelin that is mediated by complement receptor-3 (known also as MAC-1; CD11b/CD18; αMβ2 integrin) and SRA (scavenger receptor-AI/II). Observations suggest that Galectin-3/MAC-2 may act as a molecular switch that activates phagocytosis by up-regulating and prolonging KRas-GTP-dependent PI3K (phosphatidylinositol 3-kinase) activity. A similar mechanism may regulate the phagocytosis of other tissue debris, neurotoxic factors and pathogens in neurodegenerative and infectious diseases.
AB - Microglia are a self-sustained population of immune/myeloid cells present throughout the central nervous system (CNS). Microglia are in a "resting" state in the normal adult CNS. They turn "active" in injury and disease (e.g., trauma, neurodegeneration, and infection). Activated microglia can be beneficial as well as detrimental/neurotoxic. The innate-immune function of phagocytosis of tissue debris, neurotoxic factor, and pathogens is a beneficial function of microglia. The current manuscript reviews the role of Galectin-3 (known also as MAC-2; Galectin-3/MAC-2) in the activation of the phagocytosis of degenerated myelin that is mediated by complement receptor-3 (known also as MAC-1; CD11b/CD18; αMβ2 integrin) and SRA (scavenger receptor-AI/II). Observations suggest that Galectin-3/MAC-2 may act as a molecular switch that activates phagocytosis by up-regulating and prolonging KRas-GTP-dependent PI3K (phosphatidylinositol 3-kinase) activity. A similar mechanism may regulate the phagocytosis of other tissue debris, neurotoxic factors and pathogens in neurodegenerative and infectious diseases.
KW - Galectin-3
KW - MAC-2
KW - Myelin
KW - Neurodegenetation
KW - Phagocytosis
KW - Wallerian degeneration
UR - http://www.scopus.com/inward/record.url?scp=74149092361&partnerID=8YFLogxK
U2 - 10.1007/s12031-009-9186-7
DO - 10.1007/s12031-009-9186-7
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C2 - 19253007
AN - SCOPUS:74149092361
SN - 0895-8696
VL - 39
SP - 99
EP - 103
JO - Journal of Molecular Neuroscience
JF - Journal of Molecular Neuroscience
IS - 1-2
ER -