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dc.contributor.advisor Patschan, Daniel Prof. Dr.
dc.contributor.author Scheidmann, Roman
dc.date.accessioned 2016-12-21T07:32:06Z
dc.date.available 2017-01-18T23:50:24Z
dc.date.issued 2016-12-21
dc.identifier.uri http://hdl.handle.net/11858/00-1735-0000-002B-7CED-2
dc.language.iso deu de
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.ddc 610 de
dc.title Die Effekte von PPARα auf die therapeutische Effektivität von eEOCs beim ischämisch bedingten akuten Nierenversagen von eEOC-behandelten C57BI/6N-Mäusen de
dc.type doctoralThesis de
dc.title.translated The effects of PPARα on eEOC-based therapy in ischemic acute renal failure of eEOC-treated C57BI / 6N mice de
dc.contributor.referee Patschan, Daniel Prof. Dr.
dc.date.examination 2017-01-11
dc.description.abstracteng BACKGROUND: The aim of this work was to investigate consequences of PPARα-activation by fenofibrate and clofibrate, of murine eEOCs in a cell-based therapeutic approach to Acute Renal Failure – AKI.  In the last years it was shown that the renoprotective effect of eEOC-therapy can be improved/modulated by in vitro pre-treatment with 8-O-cAMP, melatonine, angiopoetine-1, angiopetine-2 and Bone Morphogenetic Protein-5. The therapeutic benefit of PPARα-activation in the context of renal and cardiovascular pathology has been demonstrated before. METHODS: Male C57/Bl6N mice, subjected to unilateral renal ischemia (40 min.) and post-uninephrectomy, were systemically injected with 5 × 105 untreated or fenofibrate (FF 50 μM)/clofibrate (CF 1 mM) pretreated syngeneic murine eEOCs. Renal function (serum-creatinine) was analyzed 48 h later. Cellular consequences of eEOC treatment with fibrates (FF 1, 5, 10, 50 μM, CF 1 mM) were evaluated using different in vitro assays (direct cell migration, apoptosis, cellular secretion of vascular endothelial growth factor (VEGF)). RESULTS: Administration of untreated eEOCs did not protect mice from AKI.  Injection of eEOCs treated with FF 50 μm or CF 1 mM did not result in any protection from ischemia-induced renal dysfunction.  In vitro analysis showed reduced cellular secretion of vasoprotective VEGF by CF 1 mM and FF in every concentration except for FF 10 µM. FF 50 µM increased percentages of apoptotic eEOCs, with lower FF concentrations (1, 5, 10 μM) cell survival and migration was increased. CF failed to stimulate migration of cultured cells. CONCLUSION: PPARα-activation using fibrates does not stimulate renoprotective effects of syngeneic murine eEOCs in ischemic AKI, although lower fibrate concentrations significantly activate eEOCs in vitro. de
dc.contributor.coReferee Schroeter, Marco PD Dr.
dc.contributor.thirdReferee Schön, Margarete Prof. Dr.
dc.subject.eng Acute Renal Injury de
dc.subject.eng cell-based therapy de
dc.subject.eng fibrate treatment de
dc.subject.eng PPARα de
dc.subject.eng murine eEOCs de
dc.identifier.urn urn:nbn:de:gbv:7-11858/00-1735-0000-002B-7CED-2-0
dc.affiliation.institute Medizinische Fakultät de
dc.subject.gokfull Medizin (PPN619874732) de
dc.subject.gokfull Nephrologie (PPN619875828) de
dc.description.embargoed 2017-01-18
dc.identifier.ppn 875560334

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