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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.

Abstract：

: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 7 days, 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.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Frauenknecht K,Bargiotas P,Bauer H,von Landenberg P,Schwaninger M,Sommer C

doi

10.1016/j.jneuroim.2010.05.043

subject

Has Abstract

pub_date

2010-10-08 00:00:00

pages

1-9

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(10)00252-3

journal_volume

227

pub_type

杂志文章

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