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Einfluss der Tie-2 modulierenden Angiopoetine-1 und -2 auf die nephroprotektiven Effekte endothelialer Vorläuferzellen im Mäusemodell des akuten ischämischen Nierenversagens

dc.contributor.advisorPatschan, Daniel PD Dr.de
dc.contributor.authorRinneburger, Jörgde
dc.date.accessioned2013-03-08T09:47:53Zde
dc.date.available2013-03-21T23:50:04Zde
dc.date.issued2013-03-08de
dc.identifier.urihttp://hdl.handle.net/11858/00-1735-0000-000E-0C22-Dde
dc.identifier.urihttp://dx.doi.org/10.53846/goediss-3750
dc.language.isodeude
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subject.ddc610de
dc.titleEinfluss der Tie-2 modulierenden Angiopoetine-1 und -2 auf die nephroprotektiven Effekte endothelialer Vorläuferzellen im Mäusemodell des akuten ischämischen Nierenversagensde
dc.typedoctoralThesisde
dc.title.translatedThe influence of angipoetine-1 and angiopoetine-2 to the renoprotective effect of endothelial progenitor cells in mouse modelsde
dc.contributor.refereePatschan, Daniel PD Dr.de
dc.date.examination2013-03-13de
dc.description.abstractengThe aim of this study was to evaluate the modulatory effects of Angiopoietin-1 and -2 (Ang-1, Ang-2) on endothelial progenitor cells in murine acute ischemic renal failure. Therefore, C57BI/6N male mices were subjected to acute renal ischemia of 40 minutes. Mice were either injected with untreated or Ang-1-/Ang-2-pretreated syngeneic murine EPCs (cell number per experiment: 0.5*106). Concentrations of Ang-1 and Ang-2 were chosen according to previously published results on the role of Ang-2 in the process of EPC mobilization. Cell injections were performed systemically after transient occlusion of the left renal pedicle post-uninephrectomy. Analyses were performed at 48 hours after surgery. Blood was collected from the mice's hearts by transdiaphragmal punction, followed by tissue collection for histology and immunhistology. Main parameters for the prevention of acute ischaemic renal failure were serum creatinine concentration and conventional histology in comparison to untreated controls. Neither Ang-1 nor Ang-2 improved the cells renoprotective capacity. Cell pretreatment with Ang-1 resulted in further postischemic deterioration, these effects were completely blockable by coincubating the cells with Ang-1 and a specific blocking peptide. Histological analysis showed aggravation of postischemic tissue damage in mice injected with Ang-1 pretreated EPCs. Immunofluorescence did not display increased postischemic homing of prelabelled (cell tracker®) untreated or Ang-1-/ Ang-2-pretreated cells. In summary, both proteins failed to stimulate renoprotective competence of EPCs in ARF, although comparable concentrations of Ang-2 had been shown to induce EPCs mobilization if applied to mice. The mechanims responsible for deleterious effects of Ang-1 need to be elucidated.de
dc.contributor.coRefereeWilting, Jörg Prof. Dr.de
dc.contributor.thirdRefereeSchäfer, Katrin Prof. Dr.de
dc.contributor.thirdRefereeMausberg, Rainer Prof. Dr.de
dc.subject.engRenal failurede
dc.subject.engcolony forming unit endothelial cellsde
dc.subject.engAngiopoetinde
dc.subject.engEpcde
dc.subject.engCfuecde
dc.subject.engArfde
dc.identifier.urnurn:nbn:de:gbv:7-11858/00-1735-0000-000E-0C22-D-6de
dc.affiliation.instituteMedizinische Fakultätde
dc.subject.gokfullMedizin (PPN619874732)de
dc.subject.gokfullNephrologie (PPN619875828)de
dc.description.embargoed2013-03-21de
dc.identifier.ppn750587903


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