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|Title:||Expression of macrophage colony-stimulating factor and its receptor in microglia activation is linked to teratogen-induced neuronal damage||Authors:||Hao, A.-J.
Macrophage colony-stimulating factor
Macrophage colony-stimulating factor receptor
|Issue Date:||2002||Citation:||Hao, A.-J., Dheen, S.T., Ling, E.-A (2002). Expression of macrophage colony-stimulating factor and its receptor in microglia activation is linked to teratogen-induced neuronal damage. Neuroscience 112 (4) : 889-900. ScholarBank@NUS Repository. https://doi.org/10.1016/S0306-4522(02)00144-6||Abstract:||Prenatal exposure to teratogen agents is linked to the pathogenesis of neurodevelopment disorders, but the mechanisms leading to the neurodevelopmental disturbance are poorly understood. To elucidate this, an in vitro model of microglial activation induced by neuronal injury has been characterized. In this connection, exposure of primary microglial cells to the conditioned medium from the neuronal damage induced by teratogen, cyclophosphamide, is accompanied by a reactive microgliosis as assessed by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, lectin histochemistry, double labeling immunohistochemistry and in situ hybridization. Our results showed that reactive microglia were capable of releasing various cytokines such as tumor necrosis factor-α, interleukin-1, interleukin-6, transforming growth factor-β and nitric oxide. Also, we have shown that macrophage colony-stimulating factor (M-CSF) was in fact produced by the reactive microglia. Concomitant to this was the increased expression of M-CSF receptor in these cells following the teratogen-induced neuronal injury. The up-regulation of M-CSF receptor suggests that the cells are capable of responding to self-derived M-CSF in an autocrine fashion. Results with antibody neutralization further suggest that microglial proinflammatory response, as manifested by cytokine expression in culture, is mediated by M-CSF, which acts as a molecular signal that initiates a microglial reaction. We therefore suggest that microglial activation following cyclophosphamide treatment is not only a response to the neuronal damage, but is also a cause of the damage during pathogenesis of neurodevelopment disorders. To this end, the increased expression of M-CSF and its receptor on microglia would be directly linked to the active cell proliferation and proinflammatory response in the teratogen-induced injury. © 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved.||Source Title:||Neuroscience||URI:||http://scholarbank.nus.edu.sg/handle/10635/33475||ISSN:||03064522||DOI:||10.1016/S0306-4522(02)00144-6|
|Appears in Collections:||Staff Publications|
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