Neuroprotective effect of Fn14 deficiency is associated with induction of the granulocyte-colony stimulating factor (G-CSF) pathway in experimental stroke and enhanced by a pathogenic human antiphospholipid antibody

Using a transgenic mouse model of ischemic stroke we checked for a possible interaction of antiphospholipid antibodies (aPL) which often cause thromboses as well as central nervous system (CNS) involvement under non-thrombotic conditions and the TWEAK/Fn14 pathway known to be adversely involved in i...

Full description

Saved in:
Bibliographic Details
Main Authors: Frauenknecht, Katrin Barbara Magda (Author) , Bargiotas, Panagiotis (Author) , Bauer, Henrike (Author) , Landenberg, Philipp von (Author) , Schwaninger, Markus (Author) , Sommer, Clemens (Author)
Format: Article (Journal)
Language:English
Published: 25 May 2010
In: Journal of neuroimmunology
Year: 2010, Volume: 227, Issue: 1-2, Pages: 1-9
ISSN:1872-8421
DOI:10.1016/j.jneuroim.2010.05.043
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.jneuroim.2010.05.043
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0165572810002523
Get full text
Author Notes:Katrin Frauenknecht, Panagiotis Bargiotas, Henrike Bauer, Philipp von Landenberg, Markus Schwaninger, Clemens Sommer
Description
Summary:Using a transgenic mouse model of ischemic stroke we checked for a possible interaction of antiphospholipid antibodies (aPL) which often cause thromboses as well as central nervous system (CNS) involvement under non-thrombotic conditions and the TWEAK/Fn14 pathway known to be adversely involved in inflammatory and ischemic brain disease. After 7days, infarct volumes were reduced in Fn14 deficient mice and were further decreased by aPL treatment. This was associated with strongest increase of the endogenous neuroprotective G-CSF/G-CSF receptor system. This unexpected beneficial action of aPL is an example for a non-thrombogenic action and the double-edged nature of aPL.
Item Description:Gesehen am 19.06.2023
Physical Description:Online Resource
ISSN:1872-8421
DOI:10.1016/j.jneuroim.2010.05.043