Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?

Reich, Arno; Spering, Christopher; Schulz, Jörg B.

doi:10.1016/j.tins.2008.06.007

Cited by 41 publications

(46 citation statements)

References 68 publications

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“…The influence of death receptors (DRs) on the fate of neuronal networks is complex, depending not only on cell type and disease pathology, but also on the stage of a disease (Reich et al, 2008). Fas/ CD95, the best-studied DR in the CNS (Choi and Benveniste, 2004), gives an example of how divergent the DR-mediated biological effects on neurons are.…”

Section: Introductionmentioning

confidence: 99%

“…Fas/ CD95, the best-studied DR in the CNS (Choi and Benveniste, 2004), gives an example of how divergent the DR-mediated biological effects on neurons are. In addition to its eponymous apoptotic signaling, an increasing number of nonapoptotic functions emerge (Lambert et al, 2003;Wajant et al, 2003;Peter et al, 2005;Reich et al, 2008). Recent evidence that Fas signaling positively influences processes such as malignant brain tumor progression (Kleber et al, 2008) as well as induction of neurogenesis (Ceccatelli et al, 2004;Ricci-Vitiani et al, 2004) and neuritogenesis Zuliani et al, 2006;Ruan et al, 2008) indicates its neuroplastic potential.…”

Section: Introductionmentioning

confidence: 99%

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Fas/CD95 Regulatory Protein Faim2 Is Neuroprotective after Transient Brain Ischemia

Reich¹,

Spering²,

Gertz³

et al. 2011

J. Neurosci.

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Death receptor (DR) signaling has a major impact on the outcome of numerous neurological diseases, including ischemic stroke. DRs mediate not only cell death signals, but also proinflammatory responses and cell proliferation. Identification of regulatory proteins that control the switch between apoptotic and alternative DR signaling opens new therapeutic opportunities. Fas apoptotic inhibitory molecule 2 (Faim2) is an evolutionary conserved, neuron-specific inhibitor of Fas/CD95-mediated apoptosis. To investigate its role during development and in disease models, we generated Faim2-deficient mice. The ubiquitous null mutation displayed a viable and fertile phenotype without overt deficiencies. However, lack of Faim2 caused an increase in susceptibility to combined oxygen-glucose deprivation in primary neurons in vitro as well as in caspase-associated cell death, stroke volume, and neurological impairment after cerebral ischemia in vivo. These processes were rescued by lentiviral Faim2 gene transfer. In summary, we provide evidence that Faim2 is a novel neuroprotective molecule in the context of cerebral ischemia.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fas/CD95 Regulatory Protein Faim2 Is Neuroprotective after Transient Brain Ischemia

Reich¹,

Spering²,

Gertz³

et al. 2011

J. Neurosci.

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“…Disregulated apoptosis has been implicated in neurodegenerative disorders, including Alzheimer disease, Parkinson disease, and multiple sclerosis. The FAS/FASLG system is a key regulator in neuronal cell apoptosis (Ethelland and Buhler, 2003;Reich et al, 2008). Stroke causes several neurological complications, such as hemiparalysis, dysphasia, facial palsy, and motor disorder.…”

Section: Resultsmentioning

confidence: 99%

A Promoter SNP (rs1800682, -670C/T) of FAS Is Associated with Stroke in a Korean Population

Kang¹,

Chung²,

Kim³

et al. 2010

Genomics & Informatics

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The Fas (TNF receptor superfamily, member 6) (FAS)/ FAS ligand (FASLG) interaction plays a central role in the regulation of programmed cell death. FAS and FASLG polymorphisms in promoter regions affect transcriptional activities. To investigate whether FAS and FASLG polymorphisms are associated with the development and clinical phenotypes of stroke, 2 promoter single nucleotide polymorphisms (SNPs) in FAS (rs1800682, −670C/T) and FASLG (rs763110, −844C/T) were selected and genotyped by direct sequencing in 220 stroke patients [107 ischemic stroke (IS), 77 intracerebral hemorrhage (ICH), and 36 subarachnoid hemorrhage (SAH)] and 369 control subjects. For the analysis of clinical symptoms, all stroke patients were divided into 3 clinical phenotypes according to the respective results of the National Institutes of Health Stroke Survey (NIHSS) and the Modified Barthel Index (MBI) and the presence or absence of complex regional pain syndrome (CRPS). The SNPStats, SNPAnalyzer, and Helixtree programs were used to analyze the genetic data. Multiple logistic regression models (codominant, dominant, and recessive) were used to estimate odds ratios (ORs), 95% confidence intervals (CIs), and p-values. The promoter SNP rs1800682 was associated with stroke in the codominant (OR=0.48, 95% CI=0.25-0.94, p=0.04) and dominant models (OR=0.51, 95% CI=0.30-0.87, p=0.011). However, a FASLG SNP (rs763110) was not in Hardy-Weinberg equilibrium (p＜0.05). In the analysis of stroke types, rs1800682 was associated with IS in the codominant (OR=0.30, 95% CI=0.12-0.74, p=0.025), dominant (OR=0.44, p=0.018), and recessive models (OR=0.45, 95% CI=0.21-0.99, p=0.042).The genotype frequencies of rs1800682 were different between ICH and controls in the dominant model (OR=0.49, 95% CI=0.26-0.94, p=0.031) but not between SAH and controls. In the analysis of clinical symptoms, however, rs1800682 was not related to the 3 clinical phenotypes (NIHSS, MBI, and CRPS). These results suggest that a promoter SNP (rs1800682, −670C/T) in FAS may be associated with the development of stroke in the Korean population.

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“…The first family is defined functionally as Fas inhibitory molecules and comprises 3 members (Faim1, Faim2, Faim3) that are structurally unrelated and show different expression patterns throughout the organism 1,5 . In addition, Faim2 is a member of a structurally defined family of proteins related to apoptosis named transmembrane BAX inhibitor-1 motif-containing (TMBIM) proteins, or life guard (Lfg) proteins.…”

Section: What Do We Know About Faim2?mentioning

confidence: 99%

The two sides of Faim2 -- modulation of cell death and regeneration

Falkenburger¹,

Aachen²

2017

J Neurol Neuromedicine

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Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?

Cited by 41 publications

References 68 publications

Fas/CD95 Regulatory Protein Faim2 Is Neuroprotective after Transient Brain Ischemia

Fas/CD95 Regulatory Protein Faim2 Is Neuroprotective after Transient Brain Ischemia

A Promoter SNP (rs1800682, -670C/T) of FAS Is Associated with Stroke in a Korean Population

The two sides of Faim2 -- modulation of cell death and regeneration

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