Literature DB >> 19253007

The role of Galectin-3/MAC-2 in the activation of the innate-immune function of phagocytosis in microglia in injury and disease.

Shlomo Rotshenker1.   

Abstract

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; alphaMbeta2 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.

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Year:  2009        PMID: 19253007     DOI: 10.1007/s12031-009-9186-7

Source DB:  PubMed          Journal:  J Mol Neurosci        ISSN: 0895-8696            Impact factor:   3.444


  36 in total

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Authors:  Shlomo Rotshenker
Journal:  J Mol Neurosci       Date:  2003       Impact factor: 3.444

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  55 in total

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Authors:  Wei Cai; Tuo Yang; Huan Liu; Lijuan Han; Kai Zhang; Xiaoming Hu; Xuejing Zhang; Ke-Jie Yin; Yanqin Gao; Michael V L Bennett; Rehana K Leak; Jun Chen
Journal:  Prog Neurobiol       Date:  2017-10-12       Impact factor: 11.685

Review 7.  Toll-like receptors in health and disease in the brain: mechanisms and therapeutic potential.

Authors:  Mark L Hanke; Tammy Kielian
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8.  Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis.

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