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Loss of Presenilin 2 Function Is Associated with Defective LPS-Mediated Innate Immune Responsiveness. | LitMetric

Loss of Presenilin 2 Function Is Associated with Defective LPS-Mediated Innate Immune Responsiveness.

Mol Neurobiol

Signal Transduction Laboratory, School of Biochemistry & Cell Biology, ABCRF, University College Cork, 3.41 Western Gateway Building, Western Road, Cork, Ireland.

Published: July 2016

AI Article Synopsis

Article Abstract

The importance of presenilin-dependent γ-secretase protease activities in the development, neurogenesis, and immune system is highlighted by the diversity of its substrates and characterization of Psen1- and Psen2-deficient transgenic animals. Functional differences between presenilin 1 (PS1) and presenilin 2 (PS2) are incompletely understood. In this study, we have identified a Psen2-specific function, not shared by Psen1 in Toll-like receptor signaling. We show that immortalized fibroblasts and bone marrow-derived macrophages from Psen2- but not Psen1-deficient mice display reduced responsiveness to lipopolysaccharide (LPS) with decreased nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) activity and diminished pro-inflammatory cytokine production. In whole animal in vivo responses, Psen2-deficient animals have abnormal systemic production of LPS-stimulated pro-inflammatory cytokines. Mechanistically, we demonstrate that Psen2 deficiency is paralleled by reduced transcription of tlr4 mRNA and loss of LPS-induced tlr4 mRNA transcription regulation. These observations illustrate a novel PS2-dependent means of modulating LPS-mediated immune responses and identify a functional distinction between PS1 and PS2 in innate immunity.

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Source
http://dx.doi.org/10.1007/s12035-015-9285-0DOI Listing

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