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HtrA1-dependent proteolysis of TGF-β controls both neuronal maturation and developmental survival

Launay, S., Maubert, E., Lebeurrier, N., Tennstaedt, A., Campioni, M., Docagne, F., Gabriel, C., Dauphinot, L., Potier, M. C., Ehrmann, Michael ORCID: https://orcid.org/0000-0002-1927-260X, Baldi, A. and Vivien, D. 2008. HtrA1-dependent proteolysis of TGF-β controls both neuronal maturation and developmental survival. Cell Death and Differentiation 15 (9) , pp. 1408-1416. 10.1038/cdd.2008.82

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Abstract

Transforming growth factor-β (TGF-β) signalling controls a number of cerebral functions and dysfunctions including synaptogenesis, amyloid-β accumulation, apoptosis and excitotoxicity. Using cultured cortical neurons prepared from either wild type or transgenic mice overexpressing a TGF-β-responsive luciferase reporter gene (SBE-Luc), we demonstrated a progressive loss of TGF-β signalling during neuronal maturation and survival. Moreover, we showed that neurons exhibit increasing amounts of the serine protease HtrA1 (high temperature responsive antigen 1) and corresponding cleavage products during both in vitro neuronal maturation and brain development. In parallel of its ability to promote degradation of TGF-β1, we demonstrated that blockage of the proteolytic activity of HtrA1 leads to a restoration of TGF-β signalling, subsequent overexpression of the serpin type -1 plasminogen activator inhibitor (PAI-1) and neuronal death. Altogether, we propose that the balance between HtrA1 and TGF-β could be one of the critical events controlling both neuronal maturation and developmental survival.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Subjects: Q Science > QH Natural history > QH301 Biology
Publisher: Nature Publishing Group
ISSN: 1350-9047
Last Modified: 25 Oct 2022 09:15
URI: https://orca.cardiff.ac.uk/id/eprint/57793

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