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

Katrin Frauenknecht; Panagiotis Bargiotas; Henrike Bauer; Philipp von Landenberg; Markus Schwaninger; Clemens Sommer

doi:10.1016/j.jneuroim.2010.05.043

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

Katrin Frauenknecht^*
, Panagiotis Bargiotas
, Henrike Bauer
, Philipp von Landenberg
, Markus Schwaninger
, Clemens Sommer

^*Korrespondierende/r Autor/-in für diese Arbeit

Institut für Experimentelle und Klinische Pharmakologie und Toxikologie

Department of Neuropathology
Johannes Gutenberg-Universität Mainz
Institute of Pharmacology
Universität Ulm
Ruprecht-Karls-Universität Heidelberg

13 Zitate (Scopus)

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.

Originalsprache	Englisch
Zeitschrift	Journal of Neuroimmunology
Jahrgang	227
Ausgabenummer	1-2
Seiten (von - bis)	1-9
Seitenumfang	9
ISSN	0165-5728
DOIs	https://doi.org/10.1016/j.jneuroim.2010.05.043
Publikationsstatus	Veröffentlicht - 01.10.2010

Fördermittel

The authors thank Magdeleine Herkt and Ralf Luderschmidt for technical assistance and are grateful to Astrid Wöber for editorial assistance. Transgenic Fn14 −/− mice were kindly provided by Biogen Idec. The authors are further grateful to Linda Burkly for critical reading of the manuscript. The study was supported by a grant of the MAIFOR program of the Medical Faculty of the Johannes Gutenberg University Mainz .

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SDG 3 – Gesundheit und Wohlergehen

Strategische Forschungsbereiche und Zentren

Forschungsschwerpunkt: Gehirn, Hormone, Verhalten - Center for Brain, Behavior and Metabolism (CBBM)

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10.1016/j.jneuroim.2010.05.043

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Frauenknecht, K., Bargiotas, P., Bauer, H., von Landenberg, P., Schwaninger, M., & Sommer, C. (2010). 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. Journal of Neuroimmunology, 227(1-2), 1-9. https://doi.org/10.1016/j.jneuroim.2010.05.043

@article{271cd2652b0d472090e676e65072aeef,

title = "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.",

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Frauenknecht, K, Bargiotas, P, Bauer, H, von Landenberg, P, Schwaninger, M & Sommer, C 2010, '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', Journal of Neuroimmunology, Jg. 227, Nr. 1-2, S. 1-9. https://doi.org/10.1016/j.jneuroim.2010.05.043

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. / Frauenknecht, Katrin; Bargiotas, Panagiotis; Bauer, Henrike et al.
in: Journal of Neuroimmunology, Jahrgang 227, Nr. 1-2, 01.10.2010, S. 1-9.

Publikation: Beiträge in Fachzeitschriften › Zeitschriftenaufsätze › Forschung › Begutachtung

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T1 - 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

AU - Frauenknecht, Katrin

AU - Bargiotas, Panagiotis

AU - Bauer, Henrike

AU - von Landenberg, Philipp

AU - Schwaninger, Markus

AU - Sommer, Clemens

PY - 2010/10/1

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N2 - 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.

AB - 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.

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Frauenknecht K, Bargiotas P, Bauer H, von Landenberg P, Schwaninger M, Sommer C. 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. Journal of Neuroimmunology. 2010 Okt. 1;227(1-2):1-9. doi: 10.1016/j.jneuroim.2010.05.043