Experimentelle Untersuchungen zum neuroprotektiven Einfluss von endogenem Faim2 im murinen Fadenokklusionsmodell der zerebralen Ischämie

Spering, Christopher

dc.contributor.advisor	Schulz, Jörg B. Prof. Dr.
dc.contributor.author	Spering, Christopher
dc.date.accessioned	2013-11-28T10:07:20Z
dc.date.available	2014-01-14T23:50:04Z
dc.date.issued	2013-11-28
dc.identifier.uri	http://hdl.handle.net/11858/00-1735-0000-0022-5D0B-0
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-4184
dc.language.iso	deu	de
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subject.ddc	610	de
dc.title	Experimentelle Untersuchungen zum neuroprotektiven Einfluss von endogenem Faim2 im murinen Fadenokklusionsmodell der zerebralen Ischämie	de
dc.type	doctoralThesis	de
dc.title.translated	The Inﬂuence and Neuroprotective Function of Endogenous Faim2 in the Mouse Model of Cerebral Ischemia	de
dc.contributor.referee	Schulz, Jörg B. Prof. Dr.
dc.date.examination	2014-01-07
dc.description.abstracteng	Apoptosis plays a major role in neurological development, diﬀerentiation and diseases. After being activated through Fas-ligands, the death receptor Fas/CD95 initiates a caspase cascade, leading to apoptosis. The activation and the signaling pathway itself have a major impact on the outcome of several neurological diseases, including cerebral ischemia. Recent studies have shown that in addition to cell death signaling, death receptors also induce proinﬂammatory responses and cell diﬀerentiation or proliferation. Identiﬁcation of a protein, which regulates the activation of death receptors and in that function potentially inﬂuences the switch between cell death and neuroregeneration, opens new therapeutic targets. In this doctoral theses, the death receptor inhibiting molecule Fas apoptotic inhibitory molecule 2 (Faim2) was identiﬁed and characterized as an important modifyer of Fas/CD95-induced signaling, priming the apoptosis pathway. To investigate this neuron-speciﬁc and evolutionary well conserved inhibitor during development and diseases, a Faim2-deﬁcient mouse had been generated. The lack of Faim2 causes an increase in stroke volume, neurological impairment and caspase activity in vivo as well as an increase in susceptibility to combined oxygen-glucose deprivation in primary neurons in vitro. While Faim2 was down regulated after cerebral ischemia, the expression of Fas/CD95 showed an increase, opening the discussion about alternative pathways inducing neurogenesis or neuronal branching through Fas/CD95 signaling, next to the death pathway, which leads to Apoptosis. In contrast, a lentiviral mediated overexpression of Faim2 decreased infarct volume and cell death again, completing the evidence that Faim2 is a neuroprotective molecule in the context of cerebral ischemia and potentially a therapeutic target.	de
dc.contributor.coReferee	Trendelenburg, George Prof. Dr.
dc.subject.ger	Faim2	de
dc.subject.ger	Apoptose	de
dc.subject.ger	Zerebrale Ischämie	de
dc.subject.ger	Caspase	de
dc.subject.ger	Fas	de
dc.subject.ger	CD95	de
dc.subject.eng	Faim2	de
dc.subject.eng	Apoptosis	de
dc.subject.eng	cerebral ischemia	de
dc.subject.eng	Fas	de
dc.subject.eng	CD95	de
dc.subject.eng	Faim2-deficiency	de
dc.subject.eng	caspase cascade	de
dc.subject.eng	death receptor	de
dc.subject.eng	neuroregeneration	de
dc.subject.eng	neurological development	de
dc.subject.eng	neurological disease	de
dc.identifier.urn	urn:nbn:de:gbv:7-11858/00-1735-0000-0022-5D0B-0-4
dc.affiliation.institute	Medizinische Fakultät	de
dc.subject.gokfull	Medizin (PPN619874732)	de
dc.subject.gokfull	Neurologie - Allgemein- und Gesamtdarstellungen (PPN619876247)	de
dc.description.embargoed	2014-01-14
dc.identifier.ppn	772760896

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Human- und Zahnmedizin [2871]

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