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|Title: ||Low-Density Lipoprotein Receptor Deficiency Attenuates Neuroinflammation through the Induction of Apolipoprotein E|
|Authors: ||Mailleux, Jo|
van Horssen, Jack
Bogie, Jeroen F. J.
Hendriks, Jerome J. A.
|Issue Date: ||2017|
|Publisher: ||FRONTIERS MEDIA SA|
|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: MOG(35-55) 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 (TNF alpha) 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.|
|Notes: ||[Mailleux, Jo; Timmermans, Silke; Nelissen, Katherine; Vanmol, Jasmine; Vanmierlo, Tim; Bogie, Jeroen F. J.; Hendriks, Jerome J. A.] Hasselt Univ, Biomed Res Inst, Diepenbeek, Belgium. [van Horssen, Jack] Vrije Univ Amsterdam, Mol Cell Biol & Immunol, Med Ctr, Amsterdam, Netherlands.|
|ISI #: ||000416523900001|
|Type: ||Journal Contribution|
|Appears in Collections: ||Research publications|
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