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KMID : 1161520050090020101
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Animal Cells and Systems
2005 Volume.9 No. 2 p.101 ~ p.105
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Molecular mechanisms of microglial deactivation by TGF-β-inducible protein βig-h3
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Kim Mi-Ok
Lee Eun-Joo H.
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Abstract
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βig?h3 is a secretory protein that is induced by TGF?β and implicated in various disease conditions including fibrosis. We have previously reported that βig?h3 expression is implicated in astrocyte response to brain injury. In this study, we further investigated potential roles of βig?h3 protein in the injured central nervous system (CNS). We specifically assessed whether the treatment of microglial cells with βig?h3 can regulate microglial activity. Microglial cells are the prime effector cells in CNS immune and inflammatory responses. When activated, they produce a number of inflammatory mediators, which can promote neuronal injury. We prepared conditioned medium from the stable CHO cell line transfected with human βig?h3 cDNA. We then examined the effects of the conditioned medium on the LPS? or IFN?γ?mediated induction of proinflammatory molecules in microglial cells. Preincubation with the conditioned medium significantly attenuated LPS?mediated upregulation of TNF?α, IL?1β, iNOS and COX?2 mRNA expression in BV2 murine microglial cells. It also reduced IFN?γ?mediated upregulation of TNF?α and COX?2 mRNA expression but not iNOS mRNA expression. Assays of nitric oxide release correlated with the mRNA data, which showed selective inhibition of LPS?mediated nitric oxide production. Although the regulatory mechanisms need to be further investigated, these results suggest that astrocyte?derived βig?h3 may contribute to protection of the CNS from immune?mediated damage via controlling microglial inflammatory responses.
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KEYWORD
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TGF-β, βig-h3, microglia, brain inflammation, cytokine
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