Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke

Ioana Inta; Katrin Frauenknecht; Henrike Dörr; Patricia Kohlhof; Tanja Rabsilber; Gerd U. Auffarth; Linda Burkly; Michel Mittelbronn; Kyungmin Hahm; Clemens Sommer; Markus Schwaninger

doi:10.1016/j.jns.2008.08.005

Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke

Ioana Inta, Katrin Frauenknecht, Henrike Dörr, Patricia Kohlhof, Tanja Rabsilber, Gerd U. Auffarth, Linda Burkly, Michel Mittelbronn, Kyungmin Hahm, Clemens Sommer, Markus Schwaninger^*

^*Corresponding author for this work

Institute of Experimental and Clinical Pharmacology and Toxicology

51 Citations (Scopus)

Abstract

Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. In this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels of the receptor Fn14 and a trend towards higher TWEAK mRNA levels. In the infarcted and peri-infarct tissue immunostaining for Fn14 was enhanced. These data show that the cytokine TWEAK and its membrane receptor Fn14 are upregulated in stroke and suggest that they contribute to stroke outcome.

Original language	English
Journal	Journal of the Neurological Sciences
Volume	275
Issue number	1-2
Pages (from-to)	117-120
Number of pages	4
ISSN	0022-510X
DOIs	https://doi.org/10.1016/j.jns.2008.08.005
Publication status	Published - 15.12.2008

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Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

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10.1016/j.jns.2008.08.005

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title = "Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke",

abstract = "Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. In this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels of the receptor Fn14 and a trend towards higher TWEAK mRNA levels. In the infarcted and peri-infarct tissue immunostaining for Fn14 was enhanced. These data show that the cytokine TWEAK and its membrane receptor Fn14 are upregulated in stroke and suggest that they contribute to stroke outcome.",

author = "Ioana Inta and Katrin Frauenknecht and Henrike D{\"o}rr and Patricia Kohlhof and Tanja Rabsilber and Auffarth, \{Gerd U.\} and Linda Burkly and Michel Mittelbronn and Kyungmin Hahm and Clemens Sommer and Markus Schwaninger",

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doi = "10.1016/j.jns.2008.08.005",

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T1 - Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke

AU - Inta, Ioana

AU - Frauenknecht, Katrin

AU - Dörr, Henrike

AU - Kohlhof, Patricia

AU - Rabsilber, Tanja

AU - Auffarth, Gerd U.

AU - Burkly, Linda

AU - Mittelbronn, Michel

AU - Hahm, Kyungmin

AU - Sommer, Clemens

AU - Schwaninger, Markus

PY - 2008/12/15

Y1 - 2008/12/15

N2 - Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. In this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels of the receptor Fn14 and a trend towards higher TWEAK mRNA levels. In the infarcted and peri-infarct tissue immunostaining for Fn14 was enhanced. These data show that the cytokine TWEAK and its membrane receptor Fn14 are upregulated in stroke and suggest that they contribute to stroke outcome.

AB - Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. In this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels of the receptor Fn14 and a trend towards higher TWEAK mRNA levels. In the infarcted and peri-infarct tissue immunostaining for Fn14 was enhanced. These data show that the cytokine TWEAK and its membrane receptor Fn14 are upregulated in stroke and suggest that they contribute to stroke outcome.

UR - https://www.scopus.com/pages/publications/55649111573

U2 - 10.1016/j.jns.2008.08.005

DO - 10.1016/j.jns.2008.08.005

M3 - Journal articles

C2 - 18793781

AN - SCOPUS:55649111573

SN - 0022-510X

VL - 275

SP - 117

EP - 120

JO - Journal of the Neurological Sciences

JF - Journal of the Neurological Sciences

IS - 1-2

ER -

Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke

Abstract

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