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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/25967

Title: Low-density lipoprotein receptor deficiency attenuates neuroinflammation through the induction of apolipoprotein
Authors: Mailleux, Jo
Timmermans, Silke
Nelissen, Katherine
Vanmol, Jasmine
Vanmierlo, Tim
Van Horssen, Jack
Bogie, Jeroen F. J.
Hendriks, Jerome J. A.
Issue Date: 2017
Citation: Frontiers in Immunology, 8, p. 1-12 (Art N° 1701)
Abstract: Objective: We aimed to determine the role of the low-density lipoprotein receptor (LDLr) in neuroinflammation by inducing experimental autoimmune encephalomyelitis (EAE) in ldlr knock out mice. Methods: MOG35–55 induced EAE in male and female ldlr−/− mice was assessed clinically and histopathologically. Expression of inflammatory mediators and apolipoprotein E (apoE) was investigated by qPCR. Changes in protein levels of apoE and tumor necrosis factor alpha (TNFα) were validated by western blot and ELISA, respectively. results: Ldlr−/−-attenuated EAE disease severity in female, but not in male, EAE mice marked by a reduced proinflammatory cytokine production in the central nervous system of female ldlr−/− mice. Macrophages from female ldlr−/− mice showed a similar decrease in proinflammatory mediators, an impaired capacity to phagocytose myelin and enhanced secretion of the anti-inflammatory apoE. Interestingly, apoE/ldlr double knock out abrogated the beneficial effect of ldlr depletion in EAE. conclusion: Collectively, we show that ldlr−/− reduces EAE disease severity in female but not in male EAE mice, and that this can be explained by increased levels of apoE in female ldlr−/− mice. Although the reason for the observed sexual dimorphism remains unclear, our findings show that LDLr and associated apoE levels are involved in neuroinflammatory processes.
URI: http://hdl.handle.net/1942/25967
DOI: 10.3389/fimmu.2017.01701
ISI #: 000416523900001
ISSN: 1664-3224
Category: A1
Type: Journal Contribution
Appears in Collections: Research publications

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