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Springer Nature [academic journals on nature.com], Cell Death & Differentiation, 10(21), p. 1588-1599, 2014

DOI: 10.1038/cdd.2014.68

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Lipocalin 2 modulates the cellular response to amyloid beta

Journal article published in 2014 by A. M. Falc??o, Jo??o Carlos Cruz Souza, S. D. Mesquita ORCID, A. C. Ferreira, A. M. Falcao, J. C. Sousa, Tiago Gil Oliveira ORCID, Margarida Correia-Neves ORCID, N. Sousa, F. Marques ORCID, Joana Almeida Palha ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

The production, accumulation and aggregation of amyloid beta (A??) peptides in Alzheimer's disease (AD) are influenced by different modulators. Among these are iron and iron-related proteins, given their ability to modulate the expression of the amyloid precursor protein and to drive A?? aggregation. Herein, we describe that lipocalin 2 (LCN2), a mammalian acute-phase protein involved in iron homeostasis, is highly produced in response to A??1-42 by choroid plexus epithelial cells and astrocytes, but not by microglia or neurons. Although A??1-42 stimulation decreases the dehydrogenase activity and survival of wild-type astrocytes, astrocytes lacking the expression of Lcn2 are not affected. This protection results from a lower expression of the proapoptotic gene Bim and a decreased inflammatory response. Altogether, these findings show that A?? toxicity to astrocytes requires LCN2, which represents a novel mechanism to target when addressing AD.Cell Death and Differentiation advance online publication, 23 May 2014; doi:10.1038/cdd.2014.68.