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Astrocyte reactivity to Fas activation is attenuated in TIMP-1 deficient mice, an in vitrostudy

Ogier, Crystel, Creidy, Rita, Boucraut, José, Soloway, Paul D, Khrestchatisky, Michel, Rivera, Santiago·2005·BMC Neuroscience
DOI 10.1186/1471-2202-6-68PMC PMC1325973
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Abstract

Background: Tissue inhibitor of metalloproteinases-1 (TIMP-1) is a multifunctional secreted protein with pleiotropic actions, including the inhibition of matrix metalloproteinases (MMPs), cell death/survival and growth promoting activities. After inflammatory challenge, the levels of TIMP-1 are highly and selectively upregulated in astrocytes among glial cells, but little is know about its role in these neural cells. We investigated the influence of TIMP-1 null mutation in the reactivity of cultured astrocytes to pro-inflammatory stimuli with TNF-α and anti-Fas antibody. Results: When compared to WT, mutant astrocytes displayed an overall increased constitutive gelatinase expression and were less responsive to Fas-mediated upregulation of MMP-9, of monocyte chemoattractant protein-1 (MCP-1) and of intercellular cell adhesion molecule-1 (ICAM-1), all markers of astrocyte inflammatory response. In contrast, TNF-α treatment induced all these factors similarly regardless of the astrocyte genotype. The incorporation of 3 H-thymidin, a marker of cell proliferation, increased in wild-type (WT) astrocytes after treatment with anti-Fas antibody or recombinant TIMP-1 but not in mutant astrocytes. Finally, lymphocyte chemotaxis was differentially regulated by TNF-α in WT and TIMP-1 deficient astrocytes. Conclusion: We provide evidence that the alteration of the MMP/TIMP balance in astrocytes influences their reactivity to pro-inflammatory stimuli and that Fas activation modulates the expression of members of the MMP/TIMP axis. We hypothesise that the Fas/FasL transduction pathway and the MMP/TIMP system interact in astrocytes to modulate their inflammatory response to environmental stimuli.

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Authors
Ogier, C., Creidy, R., Boucraut, J., Soloway, P. D., Khrestchatisky, M., & Rivera, S.
Venue
BMC Neuroscience
Publisher
Springer Science and Business Media LLC
Published
2005-11-29
Volume
6
Issue
1
ISSN
1471-2202
DOI
10.1186/1471-2202-6-68
PMC
PMC1325973
Cited by
31
References
1
Language
en

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